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Journal of the American Society of Hypertension

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ISSN (Print) 1933-1711
Published by Elsevier

[2556 journals]

Hypertension in adolescence is not an independent risk factor for renal cancer: a cohort study of 918,965 males
- Abstract: Publication date: Available online 13 May 2013
  Source:Journal of the American Society of Hypertension
  Author(s): Adi Leiba , Jeremy D. Kark , Arnon Afek , Estela Derazne , Lital Keinan-Boker , Ari Shamiss , Yitshak Kreiss
  Background Hypertension has been repeatedly linked to renal cell cancer, independent of overweight and anti-hypertensive drug use, but its role remains unclear, especially within the growing group of relatively young-middle aged renal cancer patients. In order to delineate the role of hypertension in early onset renal cancer, we examined the association of blood pressure measured at age 17 with the incidence of renal cancer. Methods Sociodemographic and medical data of 918,965 adolescent males examined for fitness for military service from 1967 to 2005 were linked to the National Cancer Registry in this nationwide population-based cohort study (12,910,585 person years) to obtain cancer incidence. A single measurement of blood pressure at age 17 was stratified as optimal (<120/80), normal (≥120/80 < 130/85), high normal (≥130/85 < 140/90), or high (≥140/90). We used Cox proportional hazards modeling to estimate the hazard ratio of the blood pressure categories for renal cancer, adjusted for year of birth, body mass index, origin of parents, and height. We also assessed the role of a clinical diagnosis of persistent hypertension (n = 4223, based on multiple measurements). Results Of those who had their blood pressure recorded, 90 examinees developed renal cancer. In a multivariable model, the higher categories of blood pressure were associated with a decreased risk of renal cancer (hazard ratio, 0.32; 95% confidence interval, 0.12-0.84; P = .021 for blood pressure ≥140/90 vs < 120/80). Furthermore, there was no evidence of increased risk for those with an established diagnosis of hypertension (hazard ratio, 1.28; 95% confidence interval, 0.17-9.50; P = .81). Conclusions It is unlikely that hypertension in adolescents carries an increased risk for renal cancer.
  
  PubDate: 2013-05-15T08:34:44Z
Safety and blood pressure trajectory of short-term withdrawal of antihypertensive medications in older adults: experience from a clinical trial sample
- Abstract: Publication date: Available online 13 May 2013
  Source:Journal of the American Society of Hypertension
  Author(s): Ihab Hajjar , Meaghan Hart , Siu-Hin Wan , Vera Novak
  Background The short-term safety of and blood pressure changes after withdrawing hypertension treatment in older adults in preparation for clinical trials have not been well established. Methods Participants were enrolled in a clinical trial and antihypertensive medications were tapered over 3 weeks (week 1: reduction by 25%–50%; week 2: 50%–75%, week 3: off). Blood pressure was measured at the initial visit and after stopping all antihypertensive therapy (personnel) and twice a day during the taper phase (provided monitor). Trend analyses and linear models were used to assess changes in blood pressure. Results All participants (n = 53, mean age = 71 years, total of 1158 readings) successfully tapered their medications with no symptoms. Only 2% of the readings exceeded 180/100 mm Hg, but none were consecutive. Blood pressure gradually increased with an overall increase of 12/6 mm Hg, 95% confidence interval (4/1, 21/11). The daily increase in blood pressure was 0.2 mm Hg (standard error = 0.1) in both the systolic and diastolic blood pressure. Increases in systolic and diastolic blood pressure were comparable for all antihypertensive classes (P > .05 for all). Conclusion Short-term (<3-4 weeks) withdrawal of antihypertensive therapy in older adults with hypertension is safe and is associated with mild increases in blood pressure.
  
  PubDate: 2013-05-15T08:34:44Z
Association of sodium and potassium intake with ventricular arrhythmic burden in patients with essential hypertension
- Abstract: Publication date: Available online 7 May 2013
  Source:Journal of the American Society of Hypertension
  Author(s): Maria E. Marketou , Evangelos A. Zacharis , Fragiskos Parthenakis , George E. Kochiadakis , Spyros Maragkoudakis , Gregory Chlouverakis , Panos E. Vardas
  Background Hypertensive populations suffer from an increased susceptibility to ventricular arrhythmias and sudden cardiac death. A high-salt diet appears to be a major factor involved in cardiovascular complications in hypertension. We examined the relationship between dietary salt and potassium, as indicated by urinary sodium (UNa), urinary potassium (UK), and urinary sodium/potassium ratio (UNa/K), and the arrhythmic burden in patients with essential hypertension. Methods We included 255 consecutive adult patients with well-controlled hypertension who were being followed in the hypertension outpatient clinic of a university tertiary hospital and complained of episodes of atypical chest pain and/or palpitations. All underwent 24-hour ambulatory electrocardiograph monitoring and their UNa, UK, and UNa/K ratio from 24-hour urinary excretion specimens were evaluated. Results No significant correlation was found between premature supraventricular contractions and the parameters that were examined. However, the percentage of premature ventricular contractions (PVC%) showed a weak positive association with UNa (r = 0.2; P = .001) and a moderate negative association with UK (r = −0.396; P < .001). The partial correlation coefficient of PVC% with the UNa/UK ratio remained significant even after controlling for left ventricular mass index (r = 0.437; P < .001). Conclusions A higher UNa/UK excretion ratio is significantly associated with PVCs, indicating an increased susceptibility to ventricular arrhythmias even among hypertensives with well-controlled blood pressure. Our findings reinforce recommendations for dietary interventions in those populations.
  
  PubDate: 2013-05-10T18:58:23Z
Editorial Board
- Abstract: Publication date: May–June 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 3
  
  PubDate: 2013-04-20T23:12:30Z
Table of Contents
- Abstract: Publication date: May–June 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 3
  
  PubDate: 2013-04-20T23:12:30Z
ACE2 deficiency induced perivascular fibrosis and cardiac hypertrophy during postnatal development in mice
- Abstract: Publication date: Available online 20 April 2013
  Source:Journal of the American Society of Hypertension
  Author(s): Tomozo Moritani , Masaru Iwai , Harumi Kanno , Hirotomo Nakaoka , Jun Iwanami , Takashi Higaki , Eiichi Ishii , Masatsugu Horiuchi
  In order to investigate the role of angiotensin-converting enzyme 2 (ACE2) in cardiac development, we examined the effects of ACE2 deficiency on postnatal development of the heart using ACE2-knockout (ACE2KO) mice. Heart samples of wild type (WT; C57BL/6J) mice and ACE2KO mice were taken at 1, 4, and 10 weeks of age. In WT mice, expression of ACE2 mRNA increased from 1 week to 10 weeks. A similar increase was observed in immunostaining of ACE2 in the heart, in which ACE2 was strongly expressed in coronary arteries. Compared with WT mice, heart weight was greater in ACE2KO mice at 4 weeks, and coronary artery thickening and perivascular fibrosis were also already enhanced from 4 weeks. Consistent with the increase of fibrosis, cardiac expression of collagen and TIMP was higher, and expression of MMP was lower in ACE2KO mice at 4 weeks. In addition, TGF-β mRNA was also higher, and lower expression of PPARγ mRNA was observed at 4 weeks in ACE2KO mice. These results suggest that ACE2 plays an important role in postnatal development of the heart, and that lack of ACE2 enhances coronary artery remodeling with an increase in perivascular fibrosis and cardiac hypertrophy already around the weaning period.
  
  PubDate: 2013-04-20T23:12:30Z
Assessing the role of optometrists in the control of systemic hypertension in Saudi Arabia
- Abstract: Publication date: Available online 9 April 2013
  Source:Journal of the American Society of Hypertension
  
  The low level of awareness, treatment, and control of systemic hypertension is a global problem, but it is much more serious in Saudi Arabia. This study examines the contribution made by Saudi optometrists in detection and management of patients with systemic hypertension. We surveyed a sample of 250 optometrists practicing in Saudi Arabia to evaluate the level of knowledge and awareness of their role in combating systemic hypertension. A 48.4% response rate was obtained from practicing optometrists. Of those responding, optometrists were very positive towards the use of blood pressure (BP) monitors in optometric practice on a routine basis. Forty-six percent of the optometrists had access to a BP monitor, and about 93% of these respondents actually used the monitors during clinic consultations. Automated monitors were the most common (54%). Fifty-one percent and 49% of the optometrists reported that they did routinely question their patients about high BP and about their current BP medications, respectively. The less frequently asked question concerned the cholesterol level of the patient (21%). The tests most widely used by the optometrists while examining hypertensive patients was direct ophthalmoscopy with red free filter (56%) and the least was binocular indirect ophthalmoscopy (21%). Optometrists were more likely to refer patients suspected of systemic hypertension on the basis of elevated BP (74%) and presence of retinal hemorrhages (72%), but were less likely to refer patients with changes in arteriolar reflex (41%). The opinions were very positive towards the routine monitoring of BP within the Saudi optometry profession, as optometrists indicated that they had time within an eye examination to measure BP, it was financially rewarding (56% of respondents), and patients appreciated it (64% of respondents). Despite half of the optometrists having access to BP monitors (predominantly automated devices), many of the optometrists were unsure if they were trained enough to monitor BP in such patients. There is urgent need to train optometrists on the use of BP devices, interpretation of readings, and use of additional diagnostic tests during such eye examinations.
  
  PubDate: 2013-04-13T07:13:17Z
Impaired glucose homeostasis in non-diabetic Greek hypertensives with diabetes family history. Effect of the obesity status
- Abstract: Available online 3 April 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Arterial hypertension (AH) and diabetes mellitus (DM) are established cardiovascular risk factors. Impaired glucose homeostasis (IGH; impaired fasting glucose or/and impaired glucose tolerance) or pre-diabetes, obesity, and DM family history identify individuals at risk for type 2 DM in whom preventive interventions are necessary. The aim of this study was to determine the glycemic profile in non-diabetic Greek adult hypertensive men and women according to DM family history and the obesity status. Diabetes family history, obesity markers (waist-to-hip ratio, WHR; body mass index, BMI), glycemic parameters (fasting and 2-hour post-load plasma glucose, if necessary; glycated hemoglobin, HbA1c; fasting insulin), insulin resistance indices (homeostasis model assessment, HOMA; quantitative insulin sensitivity check index, QUICKI; Bennett; McAuley), and IGH prevalence were determined in a large cohort of 11,540 Greek hypertensives referred to our institutions. Positive DM family history was associated with elevated fasting glucose (98.6 ± 13.1 vs 96.5 ± 12.3 mg/dL), HbA1c (5.58% ± 0.49% vs 5.50% ± 0.46%), fasting insulin (9.74 ± 4.20 vs 9.21 ± 3.63 μU/mL) and HOMA (2.43 ± 1.19 vs 2.24 ± 1.01) values, lower QUICKI (0.342 ± 0.025 vs 0.345 ± 0.023), Bennett (0.285 ± 0.081 vs 0.292 ± 0.078) and McAuley (6.73 ± 3.43 vs 6.95 ± 3.44) values, and higher IGH prevalence (45.3% vs 38.7%); P < .01 for all comparisons. The difference in the prevalence of IGH according to DM family history was significant (P < .01) in both genders and every WHR and BMI subgroup (except for women with BMI <20 kg/m2). Non-diabetic hypertensives with positive DM family history present with higher IGH prevalence and worse glycemic indices levels compared with those with negative family history, especially in the higher WHR/BMI subgroups.
  
  PubDate: 2013-04-05T21:30:05Z
Early predictors of alterations in left atrial structure and function related to left ventricular dysfunction in asymptomatic patients with hypertension
- Abstract: Available online 26 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Our aim was to investigate the relationships between left atrial (LA) structural and functional changes and left ventricular (LV) dysfunction related to LV pressure overload in asymptomatic patients with hypertension. One hundred and twenty-six asymptomatic patients with hypertension and LV ejection fraction (EF) ≥60% were studied. Conventional, pulsed and tissue Doppler, and two-dimensional speckle-tracking echocardiography (2DSTE) were performed to seek the independent determinants for alterations in LA structure and function. LA volume index (LAVI) correlated with age, body mass index (BMI), end-diastolic ventricular septal thickness (VSth), end-diastolic LV posterior wall thickness, relative LV wall thickness (RWT), LV mass index, peak A velocity of transmitral flow, E/e’, and peak systolic and early diastolic LA strains and strain rates. Peak LA strain during ventricular systole (S-LAs) correlated with age, BMI, heart rate (HR), end-systolic LV diameter, LAVI, VSth, RWT, LVEF, e’, E/e’, peak systolic LV radial strain, and peak early diastolic LV longitudinal strain rate. Multivariate regression analyses indicated that LV mass index, peak A velocity, E/e’, and S-LAs are defined as strong predictors related to LAVI, and that BMI, HR, LAVI, and peak systolic LV radial strain are defined as strong predictors related to S-LAs. In conclusion, 2DSTE demonstrated that alterations in LA structure and function are mainly associated with LV diastolic and systolic dysfunction, respectively, in preclinical patients with hypertension.
  
  PubDate: 2013-03-28T16:31:03Z
Intracellular angiotensin II increases the total potassium current and the resting potential of arterial myocytes from vascular resistance vessels of the rat. Physiological and pathological implications
- Abstract: Available online 26 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  The influence of intracellular and extracellular administration of angiotensin II (Ang II; 10−9 M) on total potassium current of arterial myocytes isolated from mesenteric arteries of Sprague Dawley rats was investigated. Measurements of total potassium current were performed using the voltage clamp whole cell configuration while the effect of intracellular Ang II on the resting potential of arterial myocytes was measured using the current clamp configuration of pCLAMP. The results indicated that: 1) intracellular Ang II (10−9 M) increased the total potassium current by 73% ± 2.6% (n = 22; P < .05) within 5 minutes; 2) concurrently with the increment of potassium current, the resting potential was increased by 7 ± 1.5 mV (n = 23; P < .05); 3) extracellular administration of Ang II (10−9 M) reduced the total potassium current by 20% ± 1.6% (n = 21; P < .05) within 5 minutes and depolarized the smooth muscle cells by 9 ± 2.3 mV (n = 26; P < .05); 4) the effects of intracellular Ang II on potassium current and membrane potential were inhibited by dialyzing a PKA inhibitor (10-9 M) inside the cell together with Ang II (10−9 M; P > .05); 5) valsartan (10−9 M) dialyzed into the cell together with Ang II (10−9 M) abolished the effect of the peptide on potassium current and membrane potential. The presence of endogenous or internalized intracellular Ang II in vascular resistance vessels and its effect on potassium current and resting potential indicates that the peptide present inside the arterial myocytes plays an important role on the regulation of vascular tone and consequently on peripheral resistance, which is a determining factor in the regulation of arterial blood pressure.
  
  PubDate: 2013-03-28T16:31:03Z
Outside and inside angiotensin
- Abstract: Available online 28 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  PubDate: 2013-03-28T16:31:03Z
Editorial jash volume 7, issue 3
- Abstract: Available online 21 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  PubDate: 2013-03-24T06:13:50Z
Treated hypertension and the white coat phenomenon: office readings are inadequate measures of efficacy
- Abstract: Available online 21 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  To better define the prevalence of white coat hypertension (WCH) among patients with type 2 diabetes mellitus and to estimate the magnitude of white coat effect (WCE), before and after antihypertensive therapy, we gathered data from an open-label forced-titration study of a combination of antihypertensive drugs that was titrated sequentially, in the order amlodipine, olmesartan, and hydrochlorothiazide, over an 18-week period among 187 patients with type 2 diabetes mellitus. WCH was defined as daytime ambulatory blood pressure (BP) of 135/85 mm Hg or less, but clinic BP of 140/90 mm Hg or more. WCE was obtained as the mean difference between clinic and daytime ambulatory BP. At baseline, the prevalence of WCH was 12%; all but one subject had WCE of >10/5 mm Hg. After treatment, the prevalence of WCH had increased to 39% (P < .001). In the overall population, at baseline, the mean (±SD) WCE for systolic BP was 10.4 ± 10.9 mm Hg and 3.7 ± 8.6 mm Hg for diastolic BP. After treatment, the reduction in systolic WCE was 3.01 ± 0.93 (SE; P < .0001); no reduction was seen for diastolic WCE. Among patients treated with amlodipine-olmesartan combination, WCE at baseline was 11 mm Hg systolic and was attenuated to -0.9 mm Hg. Among patients treated with amlodipine-olmesartan-hydrochlorothiazide combination, systolic WCE was similar at baseline (10.1 mm Hg) and at end of therapy (8.1 mm Hg). Mean systolic difference between dual and triple therapy of 9.9 mm Hg, SE 2.98 was significant (P < .001). The drop in diastolic WCE from 6.4 with dual therapy to -1.2 with triple therapy was also significant (mean difference 7.6, SE 2.2; P < .001). In conclusion, the prevalence of WCH increases three-fold with treatment as a result of fewer patients having sustained hypertension. Thus, out-of-office BP monitoring especially among treated hypertensive patients with type 2 diabetes is necessary to provide better assessment of overall BP and response to treatment.
  
  PubDate: 2013-03-24T06:13:50Z
Telmisartan as a metabolic sartan: the first meta-analysis of randomized controlled trials in metabolic syndrome
- Abstract: Available online 21 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Telmisartan has been proposed to be a promising cardiometabolic sartan due to its unique peroxisome proliferator-activated receptor-gamma-inducing property. To determine whether telmisartan improves metabolic parameters in metabolic syndrome, we perform the first meta-analysis of randomized controlled trials (RCTs). MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through September 2012 using PubMed and OVID. Eligible studies were RCTs of telmisartan therapy enrolling individuals with metabolic syndrome and reporting metabolic parameters as outcomes. Of 31 potentially relevant articles screened initially, 10 reports of RCTs, enrolling a total of 546 patients with metabolic syndrome, were identified and included. Pooled analysis suggested significant reductions in % changes of fasting glucose (standardized mean difference, −0.51; 95% confidence interval [CI], −0.96 to −0.06; P = .03), insulin (−0.23; 95% CI, −0.40 to −0.06; P = .008), glycosylated hemoglobin (−0.26; 95% CI, −0.44 to −0.08; P = .005), and homeostasis model assessment index (−0.22; 95% CI −0.39 to −0.05; P = .01); and a significant increase in % changes of adiponectin (0.75; 95% CI, 0.40 to 1.09; P < .0001) among patients with metabolic syndrome randomized to telmisartan versus control therapy. Telmisartan therapy appears to significantly improve metabolic parameters in patients with metabolic syndrome.
  
  PubDate: 2013-03-24T06:13:50Z
Recognition and management of masked hypertension: A review and novel approach
- Abstract: Available online 21 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Failure to show benefit in some cardiovascular and renal outcome trials may be a consequence of masked hypertension, a blood pressure in the hypertensive range outside the office setting. Ambulatory blood pressure monitoring and home blood pressures obtained by the patient are superior to office blood pressure for assessing individual target-organ damage and predicting cardiovascular disease morbidity and mortality. Lastly, masked hypertension is associated with an increased risk of developing primary hypertension and can be treated with either short-acting medications or improvement of underlying causes. We review the clinical impact of masked hypertension on cardiovascular risk and progression of kidney disease. We further propose a clinical management paradigm specific for masked hypertension that needs confirmation in a clinical trial.
  
  PubDate: 2013-03-24T06:13:50Z
Seasonal variation in blood pressure is modulated by gender and age but not by BMI in a large Taiwanese population, 1996–2006
- Abstract: Available online 13 March 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Previous research has found that blood pressure tends to be higher in winter and lower in summer. The present study examined seasonal variation in blood pressure by gender, hypertension medication, age group, and body mass index using contemporary Taiwanese data. Over 400,000 health screening records collected biennially between 1996 and 2006 were used to calculate average monthly systolic (SBP) and diastolic blood pressure (DBP) measurements. Generalized estimating equations were used to estimate the difference between the highest and lowest mean monthly blood pressure measurements. Mean monthly blood pressure measurements were higher in winter than in summer for all age groups, regardless of medication for hypertension. The largest difference in mean monthly blood pressure between summer and winter months was 5.3 mm Hg (Standard error = 0.7) for SBP and 3.2 mm Hg (Standard error = 0.7) for DBP. These differences were more pronounced: in SBP than in DBP; in men than in women; and in older than in younger participants. Body mass index was not clearly associated with seasonal variation in blood pressure. Seasonal variation in blood pressure among contemporary Taiwanese populations is modest and may only approach clinical significance for the diagnosis and treatment of hypertension and the prevention of cardiovascular disease amongst older male individuals.
  
  PubDate: 2013-03-16T16:30:03Z
Editorial Board
- Abstract: March–April 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 2
  
  PubDate: 2013-03-16T16:30:03Z
Table of Contents
- Abstract: March–April 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 2
  
  PubDate: 2013-03-16T16:30:03Z
Editorial Jash Volume 7, Issue 2
- Abstract: Available online 16 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  PubDate: 2013-02-20T11:11:04Z
Effect of a fixed combination of Perindopril and Amlodipine on blood pressure control in 6256 patients with not-at-goal hypertension: the AVANT’AGE study
- Abstract: Available online 19 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  In clinical practice, general practitioners are likely to face hypertensives with uncontrolled blood pressure (BP), whose antihypertensive treatment need to be modified. In the present study, 710 general practitioners have each included the first 10 patients with not-at-goal hypertension, for whom they decided to modify their antihypertensive treatment with addition of a fixed combination of Perindopril and Amlodipine at either of its four dosages: 5/5, 5/10, 10/5, or 10/10 mg. In total, 6256 patients were included, with BP measured both at baseline and after 3 months. At the end of follow-up, a mean reduction of 20.3 ± 12.4 mm Hg in systolic BP and 11.3 ± 9.6 mm Hg in diastolic BP were observed, and 62.3% achieved successful BP control. Body mass index and waist circumference were significant determinants of both systolic and diastolic BP reductions (P ≤ .04). Moreover, in addition to baseline BP level, body mass index was the only significant determinant of BP control of systolic, diastolic BP, and of both (P ≤ .04). Addition of a fixed combination of Perindopril and Amlodipine to BP regimen was efficient, in terms of BP control, for 62.3% of those patients with not-at-goal hypertension. Furthermore, baseline BP level and obesity were important influential factors of BP control.
  
  PubDate: 2013-02-20T11:11:04Z
The relationship between ventricular-vascular uncoupling during exercise and impaired left ventricular longitudinal functional reserve in hypertensive patients
- Abstract: Available online 19 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Uncoupling between heart and vessel may be accompanied by left ventricular (LV) dysfunction during exercise. We investigated the association between ventricular-vascular uncoupling during exercise and impaired LV longitudinal functional reserve in hypertensive subjects. Supine bicycle exercise echocardiography (25-watt, 3-minute increments) was performed in 216 hypertensive patients (106 male; mean age, 58 ± 9 years). Arterial elastance (Ea), end-systolic ventricular elastance (Ees), and ventricular-vascular interaction (VVI) index (Ea/Ees) were calculated at rest and at each stage of exercise. The patients were divided into three groups according to the tertile value of VVI ratio. The VVI ratio was defined as the ratio of VVI index at 50 W exercise over VVI index at rest; normal VVI response (n = 72); borderline VVI response (n = 72); and abnormal VVI response (n = 72). There were no significant differences in conventional echo parameters, mitral inflow velocities, mitral annular early diastolic (E’) velocity, and mitral annular systolic velocity (S’) at rest among the three groups. However, E’ velocities and S’ velocities at 25 W and 50 W were significantly lower in patients with abnormal VVI response compared with those in the other groups (P = .010 at 25 W, P = .008 at 50 W in E’ velocity; P = .022 at 25 W, P = .043 at 50 W in S’ velocity). Longitudinal diastolic functional reserve index from rest to 50 W was significantly lower in patients with abnormal VVI response compared with the other groups. Ventricular-vascular uncoupling during exercise was related to impaired LV longitudinal functional reserve in hypertensive patients.
  
  PubDate: 2013-02-20T11:11:04Z
Hypertension accelerates the ‘normal’ aging process with a premature increase in left atrial volume
- Abstract: Available online 19 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Hypertension (HT) is associated with left ventricular (LV) diastolic dysfunction and consequent left atrial (LA) dilatation. We investigated changes in LA size and phasic function by decade in patients with HT. Patients with mild or moderate HT (n = 122) were compared with a case controlled normal cohort (blood pressure
  PubDate: 2013-02-20T11:11:04Z
Angiogenic cytokines in renovascular disease: do they have potential for therapeutic use'
- Abstract: Available online 19 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Experimental and clinical studies suggest that the damage of the renal microvascular function and architecture may participate in the early steps of renal injury in chronic renal disease, irrespective of the cause. This supporting evidence has provided the impetus to targeting the renal microvasculature as an attempt to interfere with the progressive nature of the disease process. Chronic renovascular disease is often associated with renal microvascular dysfunction, damage, loss, and defective renal angiogenesis associated with progressive renal dysfunction and damage. It is possible that damage of the renal microvasculature in renovascular disease constitutes an initiating event for renal injury and contributes towards progressive and later on irreversible renal injury. Recent studies have suggested that protection of the renal microcirculation can slow or halt the progression of renal injury in this disease. This brief review will focus on the therapeutic potential and feasibility of using angiogenic cytokines to protect the kidney microvasculature in chronic renovascular disease. There is limited but provocative evidence showing that stimulation of vascular proliferation and repair using vascular endothelial growth factor or hepatocyte growth factor can slow the progression of renal damage, stabilize renal function, and protect the renal parenchyma. Such interventions may potentially constitute a sole strategy to preserve renal function and/or a co-adjuvant tool to improve the success of current therapeutic approaches in renovascular disease.
  
  PubDate: 2013-02-20T11:11:04Z
Salt sensitivity: a review with a focus on non-Hispanic blacks and Hispanics
- Abstract: Available online 19 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  The purpose of this review is to summarize the available information regarding salt sensitivity particularly as it relates to non-Hispanic blacks and Hispanics and to clarify possible etiologies, especially those that might shed light on potential treatment options. In non-Hispanic blacks, there is evidence that endothelial dysfunction, reduced potassium intake, decreased urinary kallikrein excretion, upregulation of sodium channel activity, dysfunction in atrial natriuretic peptide (ANP) production, and APOL1 gene nephropathy risk variants may cause or contribute to salt sensitivity. Supported treatment avenues include diets high in potassium and soybean protein, the components of which stimulate nitric oxide production. Racial heterogeneity complicates the study of salt sensitivity in Hispanic populations. Caribbean Hispanics, who have a higher proportion of African ancestry, may respond to commonly prescribed anti-hypertensive agents in a way that is characteristic of non-Hispanic black hypertensives. The low-renin hypertensive phenotype commonly seen in non-Hispanic blacks has been linked to salt sensitivity and may indicate an increased risk for salt sensitivity in a portion of the Hispanic population. In conclusion, increased morbidity and mortality associated with salt sensitivity mandates further studies evaluating the efficacy of tailored dietary and pharmacologic treatment in non-Hispanic blacks and determining the prevalence of low renin hypertension and salt sensitivity within the various subgroups of Hispanic Americans.
  
  PubDate: 2013-02-20T11:11:04Z
Role of angiotensin II type 2 receptor during regression of cardiac hypertrophy in spontaneously hypertensive rats
- Abstract: Available online 12 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  We previously reported that the AT1 receptor antagonist valsartan and the angiotensin converting enzyme (ACE) inhibitor enalapril decrease DNA synthesis and stimulate apoptosis in interstitial fibroblasts and epicardial mesothelial cells during regression of ventricular hypertrophy in spontaneously hypertensive rats (SHR). To examine the role of the AT2 receptor in this model, we studied hearts from SHR treated with valsartan or enalapril either alone or combined with the AT2 antagonist PD123319 for 1 or 2 weeks. Apoptosis was evaluated by quantification of DNA fragmentation or by TUNEL labeling. At 1 week, valsartan significantly increased ventricular DNA fragmentation, increased apoptosis in epicardial mesothelial cells, and decreased DNA synthesis. At 2 weeks, ventricular DNA content and cardiomyocyte cross-sectional area were significantly reduced. These valsartan-induced changes were attenuated by PD123319 co-administration. However, valsartan-induced increases in apoptosis of left ventricular interstitial non-cardiomyocytes was unaffected by the AT2 blocker. Enalapril-induced changes were similar to those observed with valsartan but were not affected by co-treatment with PD123319. These results demonstrate that AT1 and AT2 receptors act in a coordinated yet cell-specific manner to regulate cell growth and apoptosis in the left ventricle of SHR during AT1 receptor blockade but not ACE inhibition.
  
  PubDate: 2013-02-15T12:08:45Z
Hemodynamic circulatory patterns in young patients with predominantly diastolic hypertension
- Abstract: Available online 8 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  To evaluate the spectrum of hemodynamic patterns in patients with isolated diastolic hypertension-predominantly diastolic hypertension, we re-analyzed a previously reported cohort of 189 non-medicated hypertensive individuals that were assessed by impedance cardiography. We selected 46 patients who were less than 50 years old and had pulse pressure less or equal than 45 mm Hg confirmed by ambulatory blood pressure monitoring. The selected cohort had a mean age of 39.7 years and was 47% men. Three distinct groups were identified: a high cardiac index (CI) “hyperdynamic” group, with normal to near normal systemic vascular resistance (SVR); an intermediate CI and SVR group; and a “vasotonic” group, with low CI and high SVR. Heart rate was similar among the three groups. Stroke volume index (SVI) was significantly higher in the hyperdynamic group (61.8, 49.7, and 39.7 mL/m2 in the high, intermediate, and low CI groups, respectively). The hyperdynamic group had greater total arterial compliance index than the vasotonic group (1.3 ± 0.3 vs 0.92 ± 0.2 mL/m2 mm Hg for high vs low CI, respectively; P < .001). In conclusion, isolated diastolic hypertension-predominantly diastolic hypertension patients can have diverse hemodynamic patterns that cannot be predicted based on peripherally measured blood pressure and heart rate alone. This hemodynamic complexity must be taken into account when considering the genetic and pathophysiologic mechanisms of hypertension.
  
  PubDate: 2013-02-11T19:01:33Z
Influence of beta-blockers on the myocardial mRNA expressions of circadian clock- and metabolism-related genes
- Abstract: Available online 6 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Daily rhythms are regulated by a master clock-system in the suprachiasmatic nucleus and by a peripheral clock-system in each organ. Because norepinephrine is one of the timekeepers for the myocardial circadian clock that influences cardiac metabolism, it is speculated that a beta-blocker may affect the circadian clock and metabolism in heart tissue. In this study, thirty mg/kg/day of propranolol (a lipophilic beta-blocker) or atenolol (a hydrophilic beta-blocker) was given orally to Wistar rats for 4 weeks. The mRNA expressions of Bmal1 and E4BP4 in heart tissue were suppressed by the beta-blockers. However, the mRNA expressions of these clock genes in the suprachiasmatic nucleus were unchanged. Myocardial mRNA expressions of lactate dehydrogenase a and pyruvate dehydrogenase kinase 4 were also suppressed by the beta-blockers. In addition, ATP content in heart tissue was significantly elevated by the beta-blockers throughout 24 hours. The effects of propranolol and atenolol did not differ significantly. This study showed for the first time that a beta-blocker affects myocardial clock gene expression. Propranolol and atenolol increased ATP content in heart tissue throughout 24 hours. The influences of beta-blockers may be negligible on the SCN, and may be independent of lipid solubility on heart tissue. It is well known that these drugs exert a protective effect against myocardial ischemia, which may be mediated by an increase in the preservation of myocardial ATP.
  
  PubDate: 2013-02-08T13:33:05Z
Serum placental growth factor as a predictor of early onset preeclampsia in overweight/obese pregnant women
- Abstract: Available online 6 February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  The purpose of this study was to analyze whether maternal serum placental growth factor (PlGF) could predict early onset preeclampsia (
  PubDate: 2013-02-08T13:33:05Z
Treatment adherence, clinical outcomes, and economics of triple-drug therapy in hypertensive patients
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  Poor antihypertensive treatment adherence adversely affects blood pressure control. We analyzed US health plan data to assess the impact of fixed- versus loose-dose triple-combination therapy on adherence, clinical, and economic outcomes. Patients initiating triple therapy with an angiotensin receptor blocker, angiotensin-converting enzyme inhibitor, or beta blocker plus amlodipine and hydrochlorothiazide comprised three cohorts. Within-cohort comparisons were made between fixed-dose combinations of two antihypertensives plus a second pill (two pills) or three separate pills. Outcomes included adherence, cardiovascular events, health care resource use, and costs for patients with ≥12 months follow-up. A total of 16,290 patients were matched. Patients receiving two pills were more likely to be adherent (P < .001) and less likely to discontinue treatment (P < .001) across all cohorts. Therapy with two versus three pills resulted in significantly lower adjusted risk of cardiovascular events (hazard ratio = 0.76, P = .005) in the beta blocker cohort only. Total adjusted health care costs were significantly lower for two- versus three-pill therapy in the beta blocker cohort only (cost ratio = 0.74 overall, P < .01; 0.71 hypertension-attributable, P < .01). In patients with hypertension requiring triple therapy, fixed-dose combinations that lower pill burden may improve adherence (seen across all cohorts) and clinical outcomes (seen in the beta blocker cohort) without increasing health care costs.
  
  PubDate: 2013-01-19T15:16:16Z
Table of Contents
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  PubDate: 2013-01-19T15:16:16Z
From the Editor
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  PubDate: 2013-01-19T15:16:16Z
Editorial Board
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  PubDate: 2013-01-19T15:16:16Z
Variation of some inflammatory markers in hypertensive patients after 1 year of olmesartan/amlodipine single-pill combination compared with olmesartan or amlodipine monotherapies
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  The purpose of this study was to evaluate a fixed olmesartan/amlodipine combination on blood pressure control, lipid profile, insulin sensitivity, and some inflammatory markers compared with single-drug monotherapy. A total of 276 hypertensive patients were randomly assigned to olmesartan 20 mg, amlodipine 10 mg, or a single pill containing olmesartan/amlodipine combination 20/5 mg for 12 months. We evaluated the following at baseline and after 6 and 12 months: body weight, body mass index, systolic (SBP) and diastolic blood pressures (DBP), fasting plasma glucose (FPG), fasting plasma insulin (FPI), lipid profile, tumor necrosis factor-α (TNF-α), retinol binding protein-4 (RBP-4), and interleukins 6 and 7 (IL-6 and IL-7). At baseline, and after 6 and 12 months, patients underwent an euglycemic, hyperinsulinemic clamp. The olmesartan/amlodipine combination provided a greater decrease of SBP and DPB compared with amlodipine and olmesartan monotherapies. The olmesartan/amlodipine combination decreased FPG after 12 months compared with amlodipine monotherapy. The combination decreased FPI and homeostasis model assessment index and increased M value both compared with baseline and with olmesartan and amlodipine monotherapies. Olmesartan/amlodipine decreased IL-7, but not IL-6, compared with single drug components. The olmesartan/amlodipine combination is effective and safe in reducing blood pressure and has some additive effects not shown by single drugs, such as an improvement of IL-7.
  
  PubDate: 2013-01-19T15:16:16Z
Long-term follow-up of patients with atherosclerotic renal artery disease
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  Atherosclerotic renal artery stenosis (ARAS) is a predictor of increased morbidity and mortality. However, whether ARAS itself accelerates the arteriosclerotic process or whether ARAS is solely the consequence of atherosclerosis is unclear. We imaged renal arteries of 1561 hypertensive patients undergoing coronary angiography and followed this cohort for 9 years (range, 2.4–15.1 years; median, 31.2 months, interquartile range, 13.4/52.9 months). All patients received aspirin, renin-angiotensin system blockade, statins, and beta blockade as indicated. One hundred seventy-one patients had ARAS >50% diameter stenosis and 126 patients an arteriosclerotic plaque (ARAP) without significant stenosis. Blood pressures were not different in ARAS, ARAP, and non-ARAS patients. After adjustment for cardiovascular risk factors by propensity scores and matched pair analysis, ARAS patients had a lower ejection fraction and more coronary artery disease (CAD) than non-ARAS patients. The same was true for brain natriuretic peptide values, troponin I, and highly sensitive C-reative protein. Over 9 years, more ARAS patients died of any cause (34% vs 23%; P < .05). The prevalence of CAD in ARAP patients was higher than in non-ARAS patients and lower than in ARAS patients. The mortality of the ARAP patients at 9 years was 37%, not different from the ARAS patients. Atherosclerotic renal artery disease appears to be a marker for the severity of atherosclerosis rather than a causative factor for atherosclerosis progression.
  
  PubDate: 2013-01-19T15:16:16Z
Impaired vasomotor function induced by the combination of hypertension and hypercholesterolemia
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  Although it is well known that endothelial function is compromised in the presence of either hypertension (HTN) or hypercholesterolemia (HCh), less is known about whether and how the combination of these risk factors (HTN+HCh) results in impaired endothelium-dependent dilation (EDD). The aims of this study were to evaluate the influence of HTN+HCh on vasomotor function and to identify the mechanisms that underlie the altered vascular reactivity elicited by HTN+HCh. Endothelium-dependent and -independent vasomotor responses of aortic vessels were studied in mice with diet-induced HCh and/or HTN induced by chronic administration of either angiotensin II (AngII) or deoxycorticosterone acetate-salt. HTN+HCh elicited an impairment of EDD that appeared between each risk factor alone. Incubation with catalase resulted in more severe EDD impairment. Each risk factor enhanced vascular H2O2 production, but a larger response was noted with HTN+HCh. An attenuated EDD was not observed in AngII type 1a receptor deficient (AT1r−/−) mice, but AT1r−/− bone marrow chimeras exhibited more profound impairment compared with wild-type. HTN+HCh does not exert an additive effect of vasomotor dysfunction compared with either risk factor alone, and both H2O2 and blood cell–associated AT1r contribute to the impaired EDD responses in mice with HTN+HCh.
  
  PubDate: 2013-01-19T15:16:16Z
Comparative effectiveness research in the “real” world: lessons learned in a study of treatment-resistant hypertension
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  Comparative effectiveness research (CER) is vital to translate new efficacious diagnostic and therapeutic approaches into effectiveness in usual clinical practice settings. Studying the practice environment in which effectiveness protocols are implemented is necessary to identify the complex challenges that can limit translation of evidence. These issues were addressed in our National Heart, Lung, and Blood Institute-funded R34, “Controlling Blood Pressure in Treatment-Resistant Hypertension (TRH): A Pilot Study.” Qualitative methods were used in this cluster (clinic)-randomized, four-arm pilot study of TRH in eight diverse, community-based practices including: (i) focus group discussions with practice staff and physicians; (ii) conference calls with physicians; and (iii) discussions with research coordinators. Sources were summarized and analyzed by content analysis. Results include data segregated into categories representing facilitators of and barriers to research. Key facilitators included: (i) early success in controlling challenging TRH patients (ii) improved management of TRH, and (iii) reimbursement for study time and expenses. Barriers included: (i) time-consuming regulatory requirements; (ii) limited training and research experience of some study coordinators; and (iii) reluctance of some physicians to refer to Hypertension Specialists. Qualitative assessment is valuable for identifying facilitators and barriers to CER. This information is important in designing and implementing CER to accelerate translation of clinical efficacy into effectiveness.
  
  PubDate: 2013-01-19T15:16:16Z
New insights into the true nature of the obesity paradox and the lower cardiovascular risk
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  Obesity is considered a major risk factor for cardiovascular disease, hypertension, and diabetes by National and International Committees. For this reason, they advocate weight loss and prevention of obesity. However, several studies in patients with established coronary artery disease (CAD), congestive heart failure, and hypertension have shown an inverse relationship between obesity and mortality, the so called “obesity paradox,” whereas other studies have not shown such a relationship. In studies showing the obesity paradox (OP), body mass index (BMI) was used, almost exclusively as an index of obesity, although is a poor discriminator of total body fatness. Recent studies using better indices of obesity such as waist circumference (WC) and waist to hip ratio (WHR) have shown that high WC and WHR were directly and positively associated with higher event rate and total mortality in these patients. Because the OP could convey the wrong message in obese patients, the validity and true nature of the OP will be examined in this concise review. A Medline search of the English literature was performed between 2000 and September 2012, and 46 pertinent articles were selected for this review. The majority of these studies do not support an OP and those that do have used almost exclusively BMI as an index of obesity. Therefore, based on recent studies using other indices of body fat distribution, such as WC and WHR, besides BMI, the true existence of OP has been questioned and needs to be confirmed by future studies.
  
  PubDate: 2013-01-19T15:16:16Z
The Mosaic Theory revisited: common molecular mechanisms coordinating diverse organ and cellular events in hypertension
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  More than 60 years ago, Dr. Irvine Page proposed the Mosaic Theory of hypertension, which states that many factors, including genetics, environment, adaptive, neural, mechanical, and hormonal perturbations interdigitate to raise blood pressure. In the past two decades, it has become clear that common molecular and cellular events in various organs underlie many features of the Mosaic Theory. Two of these are the production of reactive oxygen species and inflammation. These factors increase neuronal firing in specific brain centers, increase sympathetic outflow, alter vascular tone and morphology, and promote sodium retention in the kidney. Moreover, factors such as genetics and environment contribute to oxidant generation and inflammation. Other common cellular signals, including calcium signaling and endoplasmic reticulum stress are similarly perturbed in different cells in hypertension and contribute to components of Page’s theory. Thus, Page’s Mosaic Theory formed a framework for future studies of molecular and cellular signals in the context of hypertension, and has greatly aided our understanding of this complex disease.
  
  PubDate: 2013-01-19T15:16:16Z
Nocturia in arterial hypertension: a prevalent, underreported, and sometimes underestimated association
- Abstract: January–February 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension, Volume 7, Issue 1
  
  Nocturia is a risk factor for morbidity and mortality but is frequently overlooked and underreported by patients and unrecognized by physicians. Epidemiologic studies reported that nocturnal voiding is associated not only with aging and benign prostatic hyperplasia, but also with many other clinical conditions. The majority of epidemiologic studies reported a significant relationship between nocturia and hypertension. However, the cause-and-effect relationship between them has not been established. Some physiopathological changes in hypertension are conducive to result in nocturia. These include the effects of hypertension on glomerular filtration and tubular transport, resetting of the kidney pressure-natriuresis relationship, atrial stretch and release of atrial natriuretic peptide when congestive heart failure complicates hypertension, and peripheral edema. Another link between hypertension and nocturia is obstructive sleep apnea. Furthermore, some evidence supports the relationship between nondipping behavior of blood pressure and an increased prevalence of nocturia. The use of some classes of antihypertensive agents may result in nocturia. The present review aims to provide a comprehensive evaluation of the epidemiologic evidence and physiopathological links that correlate hypertension and nocturia. Emphasis is placed on the need to take a pro-active attitude to detect and treat this hazardous condition.
  
  PubDate: 2013-01-19T15:16:16Z
Chymase mediates angiotensin-(1-12) metabolism in normal human hearts
- Abstract: Available online 9 January 2013
  Publication year: 2013
  Source:Journal of the American Society of Hypertension
  
  Identification of angiotensin-(1-12) [Ang-(1-12)] in forming angiotensin II (Ang II) by a non-renin dependent mechanism has increased knowledge on the paracrine/autocrine mechanisms regulating cardiac expression of Ang peptides. This study now describes in humans the identity of the enzyme accounting for Ang-(1-12) metabolism in the left ventricular (LV) tissue of normal subjects. Reverse phase HPLC characterized the products of 125I-Ang-(1-12) metabolism in plasma membranes (PMs) from human LV in the absence and presence of inhibitors for chymase (chymostatin), angiotensin-converting enzyme (ACE) 1 (lisinopril) and 2 (MLN-4760), and neprilysin (SHC39370). In the presence of the inhibitor cocktail, ≥98% ± 2% of cardiac 125I-Ang-(1-12) remained intact, whereas exclusion of chymostatin from the inhibitor cocktail led to significant conversion of Ang-(1-12) into Ang II. In addition, chymase-mediated hydrolysis of 125I-Ang I was higher compared with Ang-(1-12). Negligible Ang-(1-12) hydrolysis occurred by ACE, ACE2, and neprilysin. A high chymase activity was detected for both 125I-Ang-(1-12) and 125I-Ang I substrates. Chymase accounts for the conversion of Ang-(1-12) and Ang I to Ang II in normal human LV. These novel findings expand knowledge of the alternate mechanism by which Ang-(1-12) contributes to the production of cardiac angiotensin peptides.
  
  PubDate: 2013-01-11T15:24:20Z
Cardiovascular effects of pharmacologic therapies for smoking cessation
- Abstract: Available online 21 December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension
  
  Tobacco dependence is a potent risk factor for cardiovascular (CV) diseases and, despite known harms of smoking and benefits associated with smoking cessation, approximately 20% of the adult population with CV diseases or hypertension continue to smoke. Extensive research has demonstrated that nicotine replacement, varenicline, and bupropion sustained-release are superior to placebo for short- and intermediate-term smoking cessation. Because of their mechanisms of action, some smoking cessation therapies have been thought to have the potential to increase CV risk, particularly if the pharmacotherapies are taken while individuals are still smoking. Hence, we have analytically reviewed the literature describing the CV effects of therapies for smoking cessation, particularly as they apply to patients with CV disease.
  
  PubDate: 2012-12-22T18:13:37Z
Differential blood pressure reductions by angiotensin receptor blocker plus calcium channel blocker or diuretic in elderly hypertension with or without obesity
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  We conducted the Miyazaki Olmesartan Therapy for Hypertension in the EldeRly (MOTHER) study, which suggested that there are preferable effects of an angiotensin receptor blocker (ARB), olmesartan, plus a calcium channel blocker (CCB) over the ARB plus a diuretic, in elderly patients with hypertension. In this subanalysis, we examined whether obesity influences the efficacies of these combination therapies. The study subjects were 58 hypertensive patients ages 65 to 85, who had been randomly assigned to either group treated with olmesartan plus a CCB or a diuretic and completed the treatment for 6 months. Systolic and diastolic blood pressures were reduced following these combination treatments in nonobese and obese patients. In the CCB combination, blood pressure reductions in nonobese patients were larger than in obese patients at 1 and 3 months, and serum creatinine remained unchanged despite the greater reduction of blood pressure. Meanwhile, such differences were not noted in the diuretic groups. Plasma aldosterone was significantly reduced in nonobese patients of two combination groups, but not in those with obesity. ARB plus CCB combination therapy might be preferably chosen for nonobese elderly patients, whereas the influence of obesity seems smaller in the efficacy of ARB plus a diuretic.
  
  PubDate: 2012-12-18T18:15:28Z
Urinary arginine methylation index associated with ambulatory blood pressure abnormalities in children with chronic kidney disease
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  Arginine (ARG) metabolites are interrelated and are involved in chronic kidney disease (CKD) and cardiovascular disease. Twenty-four-hour ambulatory blood pressure monitoring (ABPM) appears to correlate with cardiovascular outcomes. We investigated the relationship between ARG metabolites, and their combined ratios in urine, and the ABPM profiles of children and adolescents with CKD. This cross-sectional study included 45 children and adolescents (age, 5–18 years) with stage 1 to 4 CKD. Each child underwent office blood pressure (BP) measurements, 24-hour ABPM, and urinary ARG metabolite determinations. Seventy percent of children with CKD had abnormal 24-hour ABPM profiles, including nocturnal hypertension, increased BP load, and nondipping nocturnal BP. The urinary ARG-to-asymmetric dimethylarginine (ADMA) ratio was lower, and the ADMA-to-symmetric dimethylarginine (SDMA) ratio was higher in children with advanced CKD (stages 2–4) than those with stage 1 CKD. CKD patients with BP abnormalities also had reduced urinary ARG and dimethylamine (DMA) levels. The higher urinary (ADMA+SDMA)-to-ARG ratios were correlated to ABPM abnormalities, including increased systolic BP load and non-dipping nocturnal BP. ABPM abnormalities were significantly associated with a high urinary (ADMA+SDMA)-to-ARG ratio, suggesting the possible involvement of methylated ARG in the development of hypertension among children with CKD.
  
  PubDate: 2012-12-18T18:15:28Z
Inhibition of MCP-1/CCR2 signaling pathway is involved in synergistic inhibitory effects of irbesartan with rosuvastatin on vascular remodeling
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  Additional beneficial effects of angiotensin II type 1 (AT1) receptor blockers beyond AT1 receptor blockade have been highlighted. Irbesartan is reported to act as an antagonist of the monocyte chemoattractant protein-1 (MCP-1) receptor, C-C chemokine receptor 2 (CCR2). We examined the possible synergistic effects of the combination of irbesartan with rosuvastatin on preventing vascular remodeling focusing on the MCP-1/CCR2 pathway. We observed that administration of irbesartan and CCR2 antagonist, propagermanium, at noneffective doses, decreased the neointima with a decrease in PCNA labeling index in the injured mouse femoral artery induced by cuff placement. We also observed that administration of a noneffective dose of rosuvastatin with propagermanium decreased the neointima area, suggesting that the inhibitory effect of rosuvastatin on neointima formation is at least partly attributable to blockade of the MCP-1/CCR2 pathway. Moreover, we demonstrated that the combination of irbesartan with rosuvastatin decreased neointima formation. MCP-1 mRNA level was significantly increased in injured femoral arteries, and administration of irbesartan with rosuvastatin decreased the mRNA levels of MCP-1, TNFα, and IL-1β, and increased PPARγ mRNA expression. These results suggest that the synergistic inhibitory effects of irbesartan with rosuvastatin on neointima formation may involve attenuation of MCP-1/CCR2 signaling.
  
  PubDate: 2012-12-18T18:15:28Z
Table of Contents
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  PubDate: 2012-12-18T18:15:28Z
From the Editor
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  PubDate: 2012-12-18T18:15:28Z
Mechanical stretch reduces the effect of angiotensin II on potassium current in cardiac ventricular cells of adult Sprague Dawley rats. On the role of AT1 receptors as mechanosensors
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  The influence of mechanical stretch on the effect of angiotensin II (Ang II) on potassium current was investigated on cardiomyocytes isolated from the left ventricle of adult Sprague Dawley rats. Measurements of total potassium current were performed using the voltage clamp whole cell configuration. The results indicated: that mechanical stretch increased the potassium current appreciably, an effect inhibited by valsartan (10−8 M), which is a strong inverse agonist of AT1 receptors; Ang II (10−8 M) administered to the bath increased the potassium current by 60 ± 5.2% (n = 22) in cardiomyocytes isolated from Sprague Dawley rats; mechanical stretch (3 μm) applied in the longitudinal direction for a duration of 10 minutes, reduced the effect of Ang II (10−8 M) on potassium current to 25 ± 4.3% (n = 24); 4) Bis-1 (300 nM), which is a specific inhibitor of protein kinase C, inhibited the effect of mechanical stretch on the increment of potassium current elicited by Ang II. In conclusion, the mechanical stretch of cardiomyocytes increases the potassium currents, an effect greatly dependent on the mechanical activation of AT1 receptors independently of Ang II. In addition, the increment of potassium currents caused by Ang II was greatly reduced by mechanical stretch, an effect abolished by protein kinase C inhibition.
  
  PubDate: 2012-12-18T18:15:28Z
Editorial Board
- Abstract: November–December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension, Volume 6, Issue 6
  
  PubDate: 2012-12-18T18:15:28Z
Age-dependent regulation of renal vasopressin V1A and V2 receptors in rats with genetic hypertension: implications for the treatment of hypertension
- Abstract: Available online 14 December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension
  
  The role of arginine vasopressin (AVP) as a hypertensive hormone remains controversial. We have previously reported that intervention with a V1A receptor antagonist in 6-week-old prehypertensive spontaneously hypertensive rats (SHR) for 4 weeks attenuated the subsequent development of hypertension in adult SHR. This study assessed the age-dependent regulation of plasma AVP levels and kidney V1A and V2 receptor expression during the development of hypertension in SHR and in normotensive Sprague Dawley rats. Systolic blood pressure (SBP), plasma AVP, and plasma renin activity (PRA) and kidney V1A and V2 receptor expression were assessed. SHR were studied at three ages: prehypertensive (6 weeks), developed hypertension (10 weeks), and established hypertension (16 weeks). SBP increased with age in SHR (P < .01) and both plasma AVP (P < .01) and PRA (P < .05) were increased in 10-week-old SHR. Renal medulla V1A receptor gene expression decreased in 10-week and 16-week-old SHR (P < .01), with a reduction in V1A receptor protein in the inner medulla of 16-week-old SHR (P < .05) compared with young SHR. There was no change in V2 receptor expression during the development of hypertension. In normotensive rats, plasma AVP, PRA, and kidney V1A and V2 receptor expression were unchanged over time. These data suggest that in SHR, activation of plasma AVP and the renal V1A receptor occurs during developing hypertension, with downregulation when hypertension is established. The use of V1A receptor antagonists in prehypertension may provide a unique opportunity for the prevention of hypertension in high-risk individuals.
  
  PubDate: 2012-12-18T18:15:28Z
Exercise-induced hypertension among healthy firefighters—a comparison between two different definitions
- Abstract: Available online 14 December 2012
  Publication year: 2012
  Source:Journal of the American Society of Hypertension
  
  Different studies have yielded conflicting results regarding the association of hypertensive response to exercise and cardiovascular morbidity. We compared two different definitions of exaggerated hypertensive response to exercise and their association with cardio-respiratory fitness in a population of healthy firefighters. We examined blood pressure response to exercise in 720 normotensive male career firefighters. Fitness was measured as peak metabolic equivalent tasks (METs) achieved during maximal exercise treadmill tests. Abnormal hypertensive response was defined either as systolic blood pressure ≥ 200 mm Hg; or alternatively, as responses falling in the upper tertile of blood pressure change from rest to exertion, divided by the maximal workload achieved. Using the simple definition of a 200 mm Hg cutoff at peak exercise less fit individuals (METs ≤12) were protected from an exaggerated hypertensive response (OR 0.45, 95%CI 0.30–0.67). However, using the definition of exercise-induced hypertension that corrects for maximal workload, less fit firefighters had almost twice the risk (OR 1.8, 95%CI 1.3–2.47). Blood pressure change corrected for maximal workload is better correlated with cardiorespiratory fitness. Systolic blood pressure elevation during peak exercise likely represents an adaptive response, whereas elevation out of proportion to the maximal workload may indicate insufficient vasodilation and a maladaptive response. Prospective studies are needed to best define exaggerated blood pressure response to exercise.
  
  PubDate: 2012-12-18T18:15:28Z