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Showing 1 - 200 of 1720 Journals sorted alphabetically
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Asian Journal of Medical and Biological Research     Open Access   (Followers: 3)
Asian Journal of Nematology     Open Access   (Followers: 4)
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Atti della Accademia Peloritana dei Pericolanti - Classe di Scienze Medico-Biologiche     Open Access  
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Australian Mammalogy     Hybrid Journal   (Followers: 6)
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Avian Conservation and Ecology     Open Access   (Followers: 11)
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Batman Üniversitesi Yaşam Bilimleri Dergisi     Open Access  
Berita Biologi     Open Access   (Followers: 1)
Between the Species     Open Access   (Followers: 1)
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        1 2 3 4 5 6 7 8 | Last

Journal Cover
Advances in Organ Biology
Number of Followers: 1  
  Full-text available via subscription Subscription journal
ISSN (Print) 1569-2590
Published by Elsevier Homepage  [3159 journals]
  • Introduction: Significance of the renal circulation
    • Authors: Warwick P Anderson; Roger G Evans; Kathleen M Stevenson
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Warwick P Anderson, Roger G Evans, Kathleen M Stevenson

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09053-4
      Issue No: Vol. 9 (2017)
  • Structure of the renal circulation
    • Authors: John F Bertram
      Pages: 1 - 16
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): John F Bertram

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09054-6
      Issue No: Vol. 9 (2017)
  • Development of the renal vasculature
    • Authors: Daine Alcorn
      Pages: 17 - 34
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Daine Alcorn
      While the basic architecture of the renal vasculature has been described for a long time, the molecular signals involved in the development of the renal vasculature are beginning to be disclosed. Even though these signals are similar to those involved in vascular development throughout all organs and tissues of the body, the kidney has important local determinants of vessel development. New studies reveal that the processes of vessel development are complex and involve many molecular regulators and mechanisms. This complexity permits the development of a range of functionally different blood vessels in the kidney. Future work in this area will establish just how these different vessel phenotypes develop. Finally, normal development of the renal vessels is essential in maintaining renal function in a variety of physiological states. Understanding their development is the first stage in developing therapies for renal vascular disease.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09055-8
      Issue No: Vol. 9 (2017)
  • Cell physiology of vascular smooth muscle cells and mesangial cells and
           the impact of this on the control of renal circulation
    • Authors: Gunter Wolf
      Pages: 35 - 61
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Gunter Wolf
      Renal microvessels, due to their content of VSMC which constitute the media, may constrict or relax depending on the functional state of the VSMC. An understanding of the multiple processes influencing VSMC contraction and relaxation on a molecular level is therefore of paramount importance in appreciating the processes which finally regulate the renal circulation. The function of VSMC is fundamentally influenced by the endothelium which lines the blood vessel. EC respond to many stimuli derived from the blood such as cytokines, hormones, growth factors, mechanical stress, and signals received from the interactions with blood cells. EC may integrate all of these diverse signals and produce either vasoconstrictive or vasodilatory factors which in turn modify VSMC function. Normal VSMC function depends on an intact endothelium. Injury to the endothelium leads to direct contact of VSMC with blood cells such as platelets which release growth factors. In addition, injured EC may not produce more vasodilators which are necessary for the normal function of VSMC. The consequence is vasoconstriction and proliferation of VSMC. Proliferating VSMC fundamentally change theirphenotype, migrate toward the injured endothelium, and form a neointima. Such pathophysiological responses are typical of the atherosclerotic lesion but may also occur in renal vasculitis or during chronic hypertension. The vessel diameter is often reduced by this asymmetrically localized neointima. Although growth factors such as PDGF, being released from platelets, are important for the proliferation of VSMC, there is also increasing evidence that traditionally vasoactive factors may influence VSMC growth. A picture is emerging in which vasoconstrictors such as ANG II or ET 1 exhibit growth-promoting effects whereas vasodilatory factors function as growth suppressors. The proliferation of VSMC is, as in all cells, regulated by a complex oscillation pattern of cyclins and cdks which are potential targets for the molecular intervention in order to treat vessel disease. MC share many similar structural and functional properties with VSMC. Although MC express receptors for many vasoactive factors and have myofilaments, there is little evidence that constriction of these cells may reduce glomerular capillary lumen. In contrast, MC contraction may serve a more static mechanical action to counteract expansive forces caused by intracapillary pressure. However, vasoactive factors fundamentally influence glomerular ultrafiltration by altering the sieving characteristics of the ultrafilter. Furthermore, vasoactive factors stimulate mesangial uptake and processing of macromolecules from the blood. MC proliferation and synthesis of extracellular matrix proteins are typical features of glomerular disease leading finally to glomerulosclerosis. Capillary lumen is obstructed by newly formed extracellular matrix components compromising glomerular blood flow in glomerulosclerosis. The future development of therapeutic approaches on a molecular level to interfere with these growth factors and/or the cellular responses after binding of these factors is important for the maintenance of the renal microcirculation in many kidney diseases.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09056-x
      Issue No: Vol. 9 (2017)
  • Control of afferent and efferent arteriolar tone
    • Authors: Sadayosh Ito
      Pages: 63 - 74
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Sadayosh Ito
      The balance of vascular tone of the afferent and efferent arteriole is a crucial determinant of glomerular hemodynamics. Despite the intimate anatomical relationship of the two arterioles in the JGA, the mechanisms that regulate afferent and efferent arteriolar tone are different. In the afferent arteriole, two intrinsic mechanisms, the myogenic response and macula densa-mediated TGF, play a dominant role, maintaining the GFR at a constant level over a wide range of renal perfusion pressure. Studies have shown that these two mechanisms are modulated by NO. In addition, an interaction between TGF and Ang II seems to be essential in maintaining GFR constant despite large variations in daily intake of salt and water. In the efferent arteriole, Ang II is one major factor involved in the control of vascular resistance. In addition, recent studies have provided evidence that NO and PGs produced by the glomerulus may control resistance of the downstream efferent arteriole. Since the early segment of the efferent arteriole resides within the glomerulus, various autacoid hormones produced by the glomerulus may reach and directly act on this segment, thereby controlling the glomerular capillary pressure. Thus, it would be important to understand the differences in the mechanisms operating at the afferent and efferent arteriole, as well as their alterations in various physiological and pathological conditions.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09057-1
      Issue No: Vol. 9 (2017)
  • The intrarenal distribution of blood flow
    • Authors: Thomas L Pallone; Aurelie Edwards; Melinda S Kreisberg
      Pages: 75 - 92
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Thomas L Pallone, Aurelie Edwards, Melinda S Kreisberg
      The microvasculature of the kidney is organized in a manner that permits regional distribution of blood flow to the cortex, outer medulla, and inner medulla. The resistance elements of the cortical microcirculation include interlobular arteries, afferent arterioles, and efferent arterioles. Efferent arterioles that arise from superficial glomeruli supply blood to the cortical peritubular capillary plexus. In contrast, juxtamedullary glomeruli give rise to efferent arterioles that form the vasa recta that supply the medulla of the kidney with blood flow. Descending vasa recta are contractile vessels whose parallel arrangement within outer medullary vascular bundles suggests that they play a role in the neural and hormonal control of blood flow to the outer versus inner medulla of the kidney. Many methods have been devised in an effort to measure regional perfusion of the kidney. Early efforts relied principally on tracer accumulation or tracer transit time. More recent approaches measure either single vessel blood flow with videomicroscopy or local tissue perfusion by laser Doppler. Although no method is ideal, these various approaches have combined, through the efforts of many investigators over many years, to delineate the physiological processes that regulate regional perfusion within the kidney.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09058-3
      Issue No: Vol. 9 (2017)
  • Blood flow in the glomerular capillary network
    • Authors: Kate M Denton
      Pages: 93 - 107
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Kate M Denton
      The glomerulus is no longer considered a passive filter subject to the control of the afferent and efferent resistances alone. Rather, due to its highly complex structure (geometry, topology, and cell types present), the glomerulus is known to be able to alter Kf, although how this occurs is not fully resolved. Glomeruli have in the past been modeled on the simple assumption that a single tube of constant diameter represented the glomerular network. While this has added vastly to our understanding of glomerular dynamics, this is obviously not the case morphologically, and as such the further understanding of the control of glomerular blood flow in the future will necessitate taking into account the structure of the glomerular capillary network in the analysis of glomerular dynamics.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09059-5
      Issue No: Vol. 9 (2017)
  • Autoregulation
    • Authors: Hartmut R Kirchheim; Armin Just
      Pages: 109 - 129
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Hartmut R Kirchheim, Armin Just

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09060-1
      Issue No: Vol. 9 (2017)
  • Tubuloglomerular feedback
    • Authors: Jurgen Schnermann
      Pages: 131 - 144
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Jurgen Schnermann
      The large amounts of NaCl filtered into the renal tubule represent a latent threat to body NaCl homeostasis by their potential to overwhelm the transport capacity of the nephron. An important mechanism containing this risk is the tubuloglomerular control system which regulates salt delivery into the collecting duct system where the capacity to absorb NaCl is intrinsically low. Deviations of NaCl concentration at the macula densa cells of the nephron, whether resulting from changes in GFR or in proximal tubular absorption, are sensed and translated into changes in blood flow resistance and inverse changes in GFR. These alterations restore macula densa NaCl concentration toward its setpoint. The regulatory process in the JGA begins with a change in macula densa NaCl uptake through the Na/K/2CI cotransporter. Changes in transport then initiate events that lead to the release of a number of vasoactive autacoids such as adenosine, nitric oxide, and prostaglandins. The magnitude of the TGF response to a change in luminal NaCl concentration, the TGF sensitivity, is variable: It is high in volume-depleted states whereas a diminished sensitivity is found during extracellular volume expansion. These sensitivity changes depend on angiotensin II levels as well as other factors. TGF as a minute-to-minute stabilizer of distal salt delivery is an important determinant of NaCl excretion during fast and random perturbations of the filtration forces that are unrelated to body salt balance. Resetting of the TGF system during alterations in macula densa NaCl in the minute-to-hour range prevents the system from becoming maladaptive in response to increases or decreases in distal salt delivery which are the result of changes in extracellular fluid volume.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09061-3
      Issue No: Vol. 9 (2017)
  • Neural control of the renal circulation
    • Authors: Gerald F DiBona; Ulla C Kopp
      Pages: 145 - 155
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Gerald F DiBona, Ulla C Kopp
      All elements of the renal vasculature receive a predominant noradrenergic innervation, with norepinephrine as the functional neurotransmitter. Basal levels of efferent renal sympathetic nerve activity to the renal vasculature are low. In the basal state, decreases (renal denervation, arterial and cardiac baroreceptor stimulation) in the already low level of efferent renal sympathetic nerve activity do not increase renal blood flow or decrease renal vascular resistance. A variety of afferent reflex inputs (somatic, visceral, environmental stress) produce increases in efferent renal sympathetic nerve activity which decrease renal blood flow and increase renal vascular resistance. The renal vascular responses to activation of renal sympathetic nerves are mediated by cc.,-adrenoceptors located on the renal vascular elements. The ultimate renal vascular response is influenced by the participation of paracrine factors (angiotensin II, prostaglandins), whose secretion may be influenced by the level of efferent renal sympathetic nerve activity.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09062-5
      Issue No: Vol. 9 (2017)
  • Endocrine control of renal vasculature
    • Authors: John G McDougall; Robert DeMatteo; Clive N May; Neale A Yates
      Pages: 157 - 169
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): John G McDougall, Robert DeMatteo, Clive N May, Neale A Yates
      Circulating hormones form one of the major control systems of the kidney, both with respect to the control of the excretory process and the control of renal blood vessels. Many hormones have direct actions on the renal vessels, while the effects of others are secondary to their systemic effects. Recent studies using real-time analysis of blood flow show that not only do many hormones have organ-specific effects on the vasculature, but within the kidney itself, some hormones may have differential effects on specific vessels. Such differential effects have yet to be tested for many hormones. While a number of hormones, their agonists and antagonists have been described to affect renal blood flow, intrarenal blood flow, distribution, or GFR, it is more difficult to define any role for these systems in the normal physiological control of these parameters. Included in the latter group, however, are the glucocorticoids, angiotensin 11, and possibly AVP.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09063-7
      Issue No: Vol. 9 (2017)
  • Endothelial factors in the regulation of the renal circulation: Nitric
    • Authors: William H. Beierwaltes
      Pages: 171 - 189
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): William H. Beierwaltes
      Overall, it appears that perfusion of the kidney is particularly sensitive to the tonic vasodilator tone of endothelium-derived NO. Basal renal vascular resistance is highly dependent on NO synthesis, and the arterioles are particularly sensitive to the influence of NO. Of the various constricting factors which oppose the dilator effect of NO, angiotensin II can become a particularly important antagonist with a seemingly unique renal interaction with NO under conditions which elevate angiotensin II above normal levels. While endothelium-derived NO does not seem to participate in renal blood flow autoregulation, it does control the basal level of renal blood flow around which autoregulation operates. The neuronal isoform of NOS in the macula densa appears to have a negative influence on TGF, and under certain conditions its absence or suppression allows TGF to exert an even greater influence on renal blood flow. While NO synthesis may be impaired in some conditions or models of hypertension, endothelial dysfunction and diminished NO synthesis in resistance arterioles do not seem to be generalized predisposing conditions for hypertension. Overall, NO not only contributes to basal vascular tone and regulates renal vascular resistance, but also acts as an important regulatory vasodilating buffer against factors or conditions which would acutely or chronically increase renal resistance beyond the homeostatic state.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09064-9
      Issue No: Vol. 9 (2017)
  • Angiotensin II regulation of the renal circulation
    • Authors: Pamela K Carmines
      Pages: 191 - 205
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Pamela K Carmines

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09065-0
      Issue No: Vol. 9 (2017)
  • Endothelin and the kidney
    • Authors: Ponnal Nambi
      Pages: 207 - 218
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Ponnal Nambi
      ET has been shown to exert significant effects on glomerular, tubular, and vascular functions of the kidney. ET receptor subtypes mediating these effects of ET appear to be different in different species. ET production, metabolism as well as ET binding are altered in a number of renal diseases, and ET receptor antagonists as well as antibodies have been shown to be beneficial in these diseases. Although a number of very potent and selective ET receptor antagonists are available, the future challenge lies in our understanding of the subtype of ET receptor that is involved in different disease processes.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09066-2
      Issue No: Vol. 9 (2017)
  • Nonendothelial paracrine regulation of the renal microcirculation
    • Authors: E.W Inscho; J.D Imig; L.G Navar
      Pages: 219 - 233
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): E.W Inscho, J.D Imig, L.G Navar

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09067-4
      Issue No: Vol. 9 (2017)
  • Integrative aspects of the renal medullary circulation
    • Authors: Göran Bergström; Roger G Evans
      Pages: 235 - 253
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Göran Bergström, Roger G Evans
      The renal medulla receives only 10% of the total blood flow to the kidney, but the structure and functions of its microcirculation appear to be important for the control of renal excretory function. They also appear to be critically important in long-term blood pressure control. Renal medullary blood flow can be altered independently of changes in total renal blood flow, but the mechanisms by which medullary blood flow is controlled remain poorly understood. A wide range of hormonal factors have been identified that can alter medullary blood flow under physiological and pathological conditions. The architecture of the medullary microcirculation is a vital component of the mechanisms allowing the formation of concentrated urine. Changes in the level of medullary blood flow appear to affect the corticomedullary solute gradient and thus the urine concentrating ability of the kidney. Experimental manipulation of medullary blood flow can cause reciprocal changes in blood pressure. The mechanisms involved in these effects remain unclear, but there is at least circumstantial evidence that renal antihypertensive mechanisms, comprising pressure natriuresis and the release of a putative renal medullary depressor hormone, could be profoundly influenced by changes in medullary perfusion.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09068-6
      Issue No: Vol. 9 (2017)
  • Aging and the renal circulation
    • Authors: Ziv Greenfeld; Chris Baylis
      Pages: 255 - 274
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Ziv Greenfeld, Chris Baylis
      In the course of aging, structural alterations occur in the vasculature, ECM, and tubules of the kidney. Renal perfusion declines, due to both structural changes and vasoconstriction, and leads to reductions in GFR. Vasoconstriction develops as a result of increased renal nerve activity and possibly Ang II, and decreases in the vasodilatory prostacyclin levels. The dependence of the older kidney on vasodilatory systems, such as NO, is enhanced, possibly to counterbalance the increased vasoconstriction. ET and ANP do not appear to influence the age-related hemodynamic changes. Development of structural injury with age is extremely variable; risk factors include male gender and high caloric/protein intake. Although glomerular hypertension and hypertrophy are not essential for the production of kidney damage in aging, these factors will exacerbate the process, if present. As a result of the multiple changes taking place, the aging kidney becomes vulnerable to super-imposed diseases and event to failure.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09069-8
      Issue No: Vol. 9 (2017)
  • Fetal renal circulation
    • Authors: Eugenie R Lumbers
      Pages: 275 - 299
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Eugenie R Lumbers
      This chapter details the development of the renal vasculature, the RAS, and the neural supply to the kidney. The sensitivity of the developing kidney to disruption of the activity of the fetal RAS is described. The fetal kidney has a high RVR and a low RBF and GFR. The effects on RBF and GFR of the RSNs, vasoactive peptides, and endothelium-derived factors such as NO are described. There are several unique features about the fetal renal vascular responses. First, it appears that endothelin can mediate a vasodilator response in the fetal circulation through stimulation of NO production. Second, stimulation of RSNs after adrenoreceptor blockade causes renal vasodilation.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09070-4
      Issue No: Vol. 9 (2017)
  • The renal circulation in pregnancy
    • Authors: Eugenie R Lumbers
      Pages: 301 - 316
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Eugenie R Lumbers
      The increased RBF that occurs in pregnancy is due to equivalent relaxation of afferent and efferent arterioles so that GPF is increased. Intracapillary glomerular hydrostatic pressure (Pgc) and the ultrafiltration coefficient (Kf) are unchanged. The increase in GPF is responsible for the increase in GFR. The mechanisms responsible for these changes in glomerular hemodynamics are unknown. To some extent they occur in the pseudopregnant rat; therefore, in that species it is likely that these changes in RBF and GFR are independent of the presence of the conceptus. A number of possible endocrine/paracrine factors may be responsible. NO is a likely candidate. Blockade of NO production normalizes RBF and GFR to nonpregnant levels and produces changes in glomerular structure similar to those seen in preeclampsia.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09071-6
      Issue No: Vol. 9 (2017)
  • Renal circulation in genetic experimental hypertension
    • Authors: Alain Bataillard; Ming Lo; Jean Sassard
      Pages: 317 - 329
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Alain Bataillard, Ming Lo, Jean Sassard
      This chapter focused on rat models of genetic hypertension since (1) they are widely used and (2) they allow renal function and especially RBF to be measured with a relative accuracy. The various techniques used to obtain RBF (microspheres, pulsed Doppler, ultrasonic transit time, and laser Doppler methods) are presented with their major advantages and limitations. The most frequently used experimental conditions are described since they largely influence the data. Finally, the results obtained in various strains of genetically hypertensive rats are summarized with a special emphasis on the existence of preglomerular vasoconstriction in most of these strains, which makes them close to a “multiple, micro-Goldblatt renal hypertension”.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09072-8
      Issue No: Vol. 9 (2017)
  • Remodeling of the renal resistance vessels in hypertension
    • Authors: Karin Skov; Michael I Mulvany
      Pages: 331 - 346
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Karin Skov, Michael I Mulvany
      The possibility that the renal resistance vessels are implicated in the pathogenesis of hypertension has been confirmed in rat studies demonstrating that the renal afferent arteriole is structurally narrowed in young and adult SHR. Furthermore, it has been demonstrated, in the second generation of crossbred spontaneously hypertensive rats/normotensive rats (SHR/WKY F2 hybrids), that a narrowed afferent arteriole lumen diameter at 7 weeks is a predictor of later development of high blood pressure, indicating that structural narrowing of the renal afferent arteriole could be an important link in the pathogenesis of primary hypertension. The reduced lumen diameter of resistance vessels in hypertension which is generally found, both in humans and in animals, was originally thought to be the result of a growth process in which the media encroached into the lumen. More recently, however, it has been recognized that the narrowed lumen need not be associated with growth, but can be due to a rearrangement of the wall material around the smaller lumen. Indeed, this appears to be the case in renal afferent arterioles, where the decreased lumen is accompanied by a decrease in media cross-sectional area in SHR and could therefore rather be due to inhibited growth. There is evidence indicating that the antihypertensive effect of ACE inhibitors is mediated through renal vascular mechanisms, whereas for calcium antagonists the mechanism is more doubtful. This has been supported by the finding that the ACE inhibitor cilazapril also has a stronger effect on renal afferent arteriole structure compared to the calcium antagonist mibefradil. Moreover, in SHR, ACE inhibitors also have the most persistent effect on blood pressure after treatment withdrawal compared to other antihypertensive drugs. As an overall conclusion, the available evidence points to a key role for the structure of renal afferent arterioles in the pathogenesis of hypertension in the SHR, and the hypotensive action of ACE-inhibitor treatment. Techniques for assessing renal afferent arteriolar structure in humans are at present lacking, but urgently required if the significance of these data for essential hypertension are to be assessed.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09073-x
      Issue No: Vol. 9 (2017)
  • Renal blood flow in human diseases
    • Authors: John J Kelly; Judith A Whitworth
      Pages: 347 - 368
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): John J Kelly, Judith A Whitworth

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09074-1
      Issue No: Vol. 9 (2017)
  • Renal hemodynamics in human hypertension
    • Authors: Pieter van Paassen; Dick de Zeeuw; Paul E de Jong; Gerjan Navis
      Pages: 369 - 382
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): Pieter van Paassen, Dick de Zeeuw, Paul E de Jong, Gerjan Navis

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09075-3
      Issue No: Vol. 9 (2017)
  • Obesity, insulin resistance, and the renal circulation
    • Authors: John E Hall; Michael W Brands; Eugene W Shek; Jeffrey R Henegar
      Pages: 383 - 397
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9
      Author(s): John E Hall, Michael W Brands, Eugene W Shek, Jeffrey R Henegar
      Weight gain causes high blood pressure in many essential hypertensive patients, and may be a major cause of ESRD. Although the precise mechanisms by which obesity raises blood pressure have not been fully elucidated, weight gain is associated with increased renal tubular reabsorption of sodium and a shift of pressure natriuresis toward higher blood pressures. The increased renal tubular reabsorption is compensated for, in part, by renal vasodilation and glomerular hyperfiltration. However, chronic renal vasodilation also raises hydrostatic pressure and wall stress in the glomeruli which, along with activation of neurohumoral factors and increased lipids and glucose intolerance, may cause glomerulosclerosis and loss of nephron function in obese subjects. The mechanisms by which obesity increases tubular reabsorption and shifts pressure natriuresis toward higher blood pressures are not completely understood, but do not appear to be directly related to hyperinsulinemia. Activation of the sympathetic and renin-angiotensin systems, as well as changes in intrarenal physical forces caused by medullary compression, appear to play a key role in the pathogenesis of obesity hypertension. However, the mechanisms that initiate these changes remain a fruitful area for further investigation, especially in view of the importance of weight gain as a cause of human essential hypertension and ESRD.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)09076-5
      Issue No: Vol. 9 (2017)
  • Mechanics of smooth muscle
    • Authors: Richard A Meiss
      Pages: 1 - 48
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 8
      Author(s): Richard A Meiss
      The function of smooth muscle, in its wide variety of physiological roles in the body, requires the changing of metabolic energy into mechanical effects. The study of the means by which smooth muscle cells and tissues interact physically with the internal and external environments is the field of muscle mechanics. Although the mechanical roles of smooth muscle are many and varied, their study can be organized, guided, and simplified by using the paradigm provided by years of study of skeletal muscle. This chapter first presents the terminology, functional relationships, and standard experimental approaches that have arisen largely through the study of skeletal muscle. After treating the technical requirements for making reliable and adequate mechanical measurements of smooth muscle function, specific features of the mechanics of smooth muscle are discussed, comparing and contrasting them with the mechanical properties of skeletal muscle and pointing out the special features unique to smooth muscle. The current state of knowledge in the field is briefly surveyed, and areas of current concern and importance are highlighted.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)08002-2
      Issue No: Vol. 8 (2017)
  • Regulation of smooth muscle contraction
    • Authors: William T Gerthoffer; Janice K Larsen
      Pages: 49 - 80
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 8
      Author(s): William T Gerthoffer, Janice K Larsen
      Mammalian smooth muscle cells are contractile cells embedded in the walls of a diverse set of organs including blood vessels, the airways, the gastrointestinal system, and the urogenital system. Smooth muscles from these functionally distinct organs contract in response to a broad array of extracellular messengers including sympathetic and parasympathetic neurotransmitters, autacoids, and hormones. The pattern of contraction varies depending on the source of muscle and the stimulant. There are two general patterns of contraction commonly described as phasic and tonic, which correspond to transient and stable contractions, respectively. The primary intracellular signal for producing contraction is ionic calcium (Ca2+), which activates the Ca2+-calmodulin-dependent enzyme myosin light-chain kinase (MLCK). Activated MLCK catalyzes phosphorylation of the 20-kDa myosin light chains, which increases actin-activated ATPase activity of smooth muscle myosin II. Myosin-associated phosphatases reverse the phosphorylation reaction causing relaxation. It is thought that both the kinase and phosphatase reactions are regulated by enzymes coupled to Ca2+-dependent as well as Ca2+-independent agonist-activated signaling pathways. There is also indirect evidence that smooth muscle actin associates with several proteins that might regulate myosin II motor function and actin filament structure. The actin-binding proteins caldesmon and calponin are phosphoproteins that inhibit actomyosin ATPase in vitro. Both have been hypothesized to be phosphorylated in vivo to relieve the inhibition of actomyosin ATPase and to promote contraction or regulate cell shortening. One of the main challenges to understanding regulation of smooth muscle contraction is that the composition and structure of the contractile machinery is not fully understood. Furthermore, signal transduction pathways controlling myosin phosphatases, caldesmon, and calponin phosphorylation remain undefined.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)08003-4
      Issue No: Vol. 8 (2017)
  • Changes in the composition of myosin isoforms in smooth muscle hypertrophy
           following urinary bladder outlet obstruction
    • Authors: Samuel K Chacko; Michael DiSanto; Yongmu Zheng; Alan J Wein
      Pages: 81 - 100
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 8
      Author(s): Samuel K Chacko, Michael DiSanto, Yongmu Zheng, Alan J Wein
      The ability of smooth muscles to compensate for increased functional demand is associated with alterations in the expression and function of a number of contractile proteins and other proteins that are involved in excitation-contraction coupling and active force generation. However, continuation of the structural alterations in the muscle cells of the bladder wall leads ultimately to decreased compliance and impaired emptying. Decompensation of the bladder muscle with persistent outlet obstruction is likely to be caused by breakdown of the structure and function of proteins that form the contractile apparatus and those that enable smooth muscle cells to take up, store, and release Ca2+. This would affect the activation of the contractile apparatus. In this chapter, we review the contractile proteins that are important for force production and maintenance in smooth muscles and the effect of outlet obstruction on the expression of these proteins.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)08004-6
      Issue No: Vol. 8 (2017)
  • Stimulus-response pathways in smooth muscle contraction
    • Authors: Isabelle Gorenne; Robert S Moreland
      Pages: 101 - 120
      Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 8
      Author(s): Isabelle Gorenne, Robert S Moreland
      The stimulus-response pathways to be discussed in this chapter are the processes by which pharmacological stimuli or membrane depolarization (pharmaco- and electromechanical coupling as defined in 1969 by Somlyo and Somlyo) produce an increase in cytosolic calcium, initiate crossbridge cycling, and result in the development of force. One of the most fascinating, albeit complicating, aspects of smooth muscle is the diversity in the types of cells that mediate or modulate smooth muscle responses. Moreover, each specific category of smooth muscle, such as vascular, airway, or gastrointestinal, responds to any given mediator in a manner appropriate for the physiological function of the organ the smooth muscle lines. For example, longitudinal smooth muscle of the rat stomach responds to endothelin-1 stimulation with the typical contraction; circular smooth muscle of the rat stomach relaxes in response to endothelin-1. One can envision this contrasting response as the perfect mechanism for two muscles to work together rather than in opposition to allow for efficient mixing of gastric contents. This single example is amplified throughout the literature, clearly demonstrating that the stimulus-response pathways in smooth muscle are precisely targeted at the physiological function of the cell.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(00)08005-8
      Issue No: Vol. 8 (2017)
  • Why the Eye Is Round
    • Authors: Larry S. Liebovitch
      Pages: 1 - 19
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Larry S. Liebovitch
      An impressive characteristic about eyes is their round, spherical structure. This chapter explores the optical, mechanical, structural, phylogenic, and ontogenic reasons why eyes are round. This exploration is used as a starting point to describe how the different features of the eye are related to each other, and how the roundness is maintained by the inflow and outflow of fluid in the eye.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10001-9
      Issue No: Vol. 10 (2017)
  • Tears and Their Secretion
    • Authors: Darlene A. Dartt; Robin R. Hodges; Driss Zoukhri
      Pages: 21 - 82
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Darlene A. Dartt, Robin R. Hodges, Driss Zoukhri
      The exposed surface of the eye is continuously covered by a thin film of fluid, the tear film, which covers the entire ocular surface, including the cornea (the clear “window” of the eye) and conjunctiva (the white part of the eye, which extends under the eyelid). The tear film is a complex fluid that is secreted by several different glands surrounding the eye. The epithelial cells of the ocular surface itself also secrete components of the tear film. The action of blinking spreads the film of tears over the whole surface of the eye and mixes the tears underneath the lids. The tear film serves as an interface between the external environment and the ocular surface and is the first layer of protection for the cornea and conjunctiva. It is constantly responding to stresses that include desiccation, bright light, cold, mechanical stimulation, physical injury, noxious chemicals, and bacterial, viral, and parasitic infection. The tear film also maintains the health of the cornea and conjunctiva by providing optimal electrolyte composition, pH, nutrient levels, and a complex mix of proteins, lipids, and mucin. To respond to these various external and internal requirements, exquisite control of the volume, composition, and structure of the tear film is required. This control arises from regulating secretion from the individual orbital glands and ocular surface epithelia. Regulation of tear secretion provides an extremely stable fluid that protects and maintains the cornea and conjunctiva and ensures that the transparent cornea provides the retina with its window to the world and ensures clear vision.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10002-0
      Issue No: Vol. 10 (2017)
  • The Corneal Endothelium
    • Authors: Jorge Fischbarg
      Pages: 113 - 125
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Jorge Fischbarg
      The corneal endothelium, also called “corneal posterior epithelium” is a comparatively thin innermost layer of the cornea. This chapter discusses the shape, function, and transparency of endothelial cells and electrolyte transport by the endothelium. The corneal endothelium is placed directly in the visual pathway. Therefore, a prime imperative is that this layer be transparent. However, as anticipated above, there are other requirements for it as well. The cornea is one of the very few organs in the body without blood vessels. Hence, nutrients for the stromal cells have to come across the endothelium from the aqueous humor in the anterior chamber. The chapter also discusses the the mechanism underlying fluid transport. The mechanism by which fluid would be osmotically transported by way of small local osmotic gradients is known as “local osmosis.” It is a popular explanation, in fact the predominant one, frequently found in textbooks. However, an in‐depth examination of the consequences of such mechanism for the corneal endothelial layer finds problems with it.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10004-4
      Issue No: Vol. 10 (2017)
  • Ciliary Body and Ciliary Epithelium
    • Authors: Nicholas A. Delamere
      Pages: 127 - 148
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Nicholas A. Delamere
      The ciliary body is a complex, highly specialized tissue that comprises several cell types. The ciliary muscle is situated at the base of the ciliary body and ligaments originating in the ciliary body attach to the lens. Contraction or relaxation of the muscle alters tension on the lens causing it to alter shape and thus shift focus. The surface of ciliary body is elaborated into a series of ridges named ciliary processes. Each ciliary process contains a complicated network of blood vessels that appear leaky to plasma constituents. The ciliary processes are covered by a specialized epithelium bilayer that comprises two distinct epithelial cell types, pigmented ciliary epithelium (PE) and nonpigmented ciliary epithelium (NPE). The ciliary epithelium bilayer constitutes a diffusion barrier between the blood and the aqueous humor in the interior of the eye. Barrier function depends on tight junctions between adjacent NPE cells. The ciliary body is responsible for the production of aqueous humor, a task that requires the polarized cellular distribution and coordinated function of Na, K-ATPase, Na/K/2Cl cotransporter, Na-H exchanger chloride channels and aquaporins in the NPE and PE. There is evidence suggesting an important role for gap junctions between the NPE and PE layers. The rate of aqueous humor secretion can be modified by ion transport inhibitors, by agents that modify gap junction permeability and by maneuvers that change blood flow in the ciliary processes.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10005-6
      Issue No: Vol. 10 (2017)
  • The Retinal Pigment Epithelium
    • Authors: Morten la Cour; Tongalp Tezel
      Pages: 253 - 272
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Morten la Cour, Tongalp Tezel
      The retinal pigment epithelium (RPE) is a monolayer of cuboidal epithelial cells intercalated between the photoreceptors and the choriocapillaries. The human RPE incorporates some 3.5 million epithelial cells arranged in a regular hexagonal pattern. The density of RPE cells is relatively uniform throughout the retina, approximately 4000 cells/mm2. With age, the cell density decreases particularly in the periphery, where it is reduced to approximately 2000 cells/mm2 in individuals over 40 years. The peripheral RPE cells are larger and more pleomorphic than central cells (Harman et al., 1997; del Priore et al., 2002). In the primate retina, each RPE cell faces 30–40 photoreceptors, a number that is rather constant throughout the retina, although perhaps somewhat lower in the fovea (Robinson and Hendrickson, 1995). In fully developed primate retinas, no mitoses are seen in the RPE, and the epithelium is currently believed to consist of a stable, nondividing, pool of cells (Tso and Friedman, 1967). The retinal membrane of the RPE faces the subretinal space, which is the extracellular space surrounding the photoreceptor outer segments (Figure 1). Between the optic disc and the ora serrata, there are no anatomical contacts between the photoreceptors and the RPE. The RPE forms numerous long microvilli that interdigitate with the rod outer segments. In mammals, the cone outer segments are ensheathed by multilamellar specializations of the RPE, the so‐called cone sheaths. The epithelial cells are bound together by junctional complexes with tight junctions that separate the cells into an apical half that faces the retina and a basal half that faces the choroid. The nucleus and mitochondriae are located in the basal half of the cell. Numerous pigment granules, located predominantly in the apical cytoplasm, give the epithelium its macroscopic black appearance, from which it derives its name. The choroidal side of the RPE directly apposes Bruch's membrane, a pentalaminar, approximately 2 μm thick, elastic membrane. The innermost part of Bruch's membrane is the basement membrane of the RPE. The outer part of Bruch's membrane is the basement membrane of the choriocapillaries. In between are two collagenous layers and a central elastic layer.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10009-3
      Issue No: Vol. 10 (2017)
  • The Choroid and Optic Nerve Head
    • Authors: Jens Folke Kiilgaard; Peter Koch Jensen
      Pages: 273 - 290
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Jens Folke Kiilgaard, Peter Koch Jensen
      This chapter discusses the choroidal circulation and the circulation of the optic disc. In humans, the choroidal circulation is derived from the ophthalmic artery that branches into the central retinal artery and the main posterior ciliary arteries and several anterior ciliary arteries. One to five main posterior ciliary arteries usually supply the choroid. These main posterior ciliary arteries run anteriorly along the optic nerve. Blood flow to the optic disc is obtained from three sources, classically described as supplying three distinct layers of optic nerve head tissue. The immediate retrobulbar part of the optic nerve is supplied from the central retinal artery. The chapter also discusses the innervation of the choroid and the choroidal blood flow measurements. Direct clinical measurement of choroidal blood is currently not feasible. Only indirect methods are available. These include Doppler measurements of velocity of blood flow either by ultrasound in the ciliary arteries or diode‐laser light in the submacular choroidal vasculature.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10010-x
      Issue No: Vol. 10 (2017)
  • Innate and Adaptive Immunity of the Eye
    • Authors: Mogens Holst Nissen; Carsten Röpke
      Pages: 291 - 305
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Mogens Holst Nissen, Carsten Röpke
      The “immune privileged” status of the eye is believed to be based on five different mechanisms including: (1) the blood-ocular barrier, (2) the absence of lympha tic drainage from the eye, (3) soluble factors with immune regulatory properties in ocular fluids, (4) the expression of immune regulatory molecules on the epithelial cells lining the interior of the eye, and (5) tolerance inducing antigen presenting cells (APC). This chapter describes some of these mechanisms. Avoiding intraocular infection and inflammation are of paramount importance to preserve the vision. Different strategies are employed to achieve this goal. Intraocular elimination of pathogens requires a fine balance of the immune system in strictly controlled manner to avoid permanent damage to the delicate structures of the eye. Experimental work during the last decades has disclosed a surprising complexity of regulation. These investigations have primarily focused on the anterior segment of the eye so far, but recent experiments have elucidated some of the strategies that have been used for the posterior segment of the eye.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10011-1
      Issue No: Vol. 10 (2017)
  • Drug Delivery to the Eye
    • Authors: Ashim K. Mitra; Banmeet S. Anand; Sridhar Duvvuri
      Pages: 307 - 351
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Ashim K. Mitra, Banmeet S. Anand, Sridhar Duvvuri
      This chapter provides a general insight into the past, present, and future trends in the area of ocular drug delivery. The chapter also presents a discussions on ocular barriers to drug delivery, modes of drug administration to the eye, effect of ocular fluid dynamics, transporter targeted drug delivery, and strategies to exploit transporters in enhancing ocular drug bioavailability. Ocular pathologies can cause discomfort and anxiety in patients, with the ultimate fear of loss of vision or even facial disfigurement. In spite of the continued effort directed toward the improvement and optimization of ocular drug delivery systems a progress in this area did not appear to take place at a fast pace that is typical of other delivery routes—oral, transdermal, and transmucosal. A cautious advancement is evidently imposed by the delicate nature of the eye and many restraints imposed by its anatomy and physiology.

      PubDate: 2017-12-12T09:30:58Z
      DOI: 10.1016/s1569-2590(05)10012-3
      Issue No: Vol. 10 (2017)
  • List of Contributors
    • Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10

      PubDate: 2017-12-12T09:30:58Z
  • The Cornea
    • Authors: Niels Ehlers; Jesper Hjortdal
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Niels Ehlers, Jesper Hjortdal
      The cornea is the anterior, transparent part of the collagenous wall of the eyeball. It is the window of the eye to the outer world. Its properties allow for the formation of an optical image on the light‐sensitive retina in the back of the eye. This requires transparency and regularity, but it also demands that the gross dimensions of the eye be kept constant. A regulated hydrostatic pressure within a relatively stiff eyeball accomplishes this. The aim of this chapter is to describe the human cornea. Regarding dimensions, there are of course large species variations. Functional aspects have often been studied in animal corneas and usually extended to all other species. Unless otherwise stated the text applies to the “standard human cornea”.

      PubDate: 2017-12-12T09:30:58Z
  • The Lens
    • Authors: Guido Zampighi
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Guido A. Zampighi
      The principal function of the lens and the cornea is to focus light on the retina, thus allowing the central nervous system to receive complex representations of the outside world. In all vertebrate lenses, this function is achieved by highly elongated cells called “fibers” grouped together in a mass that is transparent, deformable, and capable of maintaining homeostasis for the life of the animal. To meet these stringent requirements, nature developed ingenious evolutionary adaptations to increase the cytoplasms' refraction index and to transport ions and nutrients to fibers within the lens interior. Present hypothesis proposes that the lens creates an “internal circulatory system” that links the transport of ions and water to the movement of nutrients and waste products. These fluxes balance the conflicting requirements of attaining a large spherical shape, transparency, and maintaining homeostasis of fibers placed far from their blood supply. Another hypothesis proposes that the lens epithelium generates a fluid transport from the aqueous humor into and through the lens, which contributes to nutrient transport and waste removal.

      PubDate: 2017-12-12T09:30:58Z
  • The Vitreous
    • Authors: Henrik Sebag; Birgit Sander Morten Cour
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Henrik Lund‐Andersen, J. Sebag, Birgit Sander, Morten La Cour
      The vitreous body supports the retina, and is probably necessary for the maintenance of the clarity of the lens. Via anomalous posterior vitreous detachment (PVD) vitreoretinal pathology can have devastating consequences for visual function, and removal of pathological vitreous by vitrectomy is a common surgical procedure. This chapter discusses the anatomy, and molecular organization of the vitreous, as well as its development and aging changes. The vitreous is optically homogenous when examined in vivo with the slit lamp or by dark-field microscopy, in enucleated eyes. Aging results in structural changes in the vitreous, as well as characteristic alterations in the strength of vitreoretinal adhesion. Aging results in alterations in the strength of vitreoretinal adhesion that characteristically are unevenly distributed across the vitreoretinal interface. In the posterior part of the eye, there is a progressive weakening of the vitreoretinal adhesion. In the anterior part of the eye, increasing age is associated with remarkable changes in the vitreal base.

      PubDate: 2017-12-12T09:30:58Z
  • The Retina
    • Authors: Morten Cour; Berndt Ehinger
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Morten la Cour, Berndt Ehinger
      All vertebrate eyes have a retina, but its structure can vary immensely, and there can be significant differences, even between animal species as closely related as different primates. This chapter emphasizes on the human retina. The retina receives its photosensory input from its light‐sensitive cells, the photoreceptors. The retinal output is produced by the ganglion cells, which send their axons to the brain via the optic nerve. The intercalated neurons mediate and modulate the flow of information between the photoreceptors and the ganglion cells. A key concept in visual physiology is the receptive field of a ganglion cell or any other neuron in the visual system. The receptive field for a given cell is defined as the area in the visual field, or the region of the retinal surface, where light stimulation elicits a change in the electrical activity of the cell. The chapter discusses the individual cells and synaptic layers of the retina.

      PubDate: 2017-12-12T09:30:58Z
  • The Sclera
    • Authors: Klaus Trier
      Abstract: Publication date: 2005
      Source:Advances in Organ Biology, Volume 10
      Author(s): Klaus Trier
      The sclera is the skeleton of the eye. It defines the size of the eye, provides a stable support for its optical elements, and is essential to the achievement of a focused retinal image. The sclera provides attachment for the extraocular muscles and allows passage of vital structures such as the optic nerve, the arterial blood supply, and the venous drainage system. The overall elastic properties of the sclera neutralize short‐term fluctuations of the intraocular pressure. More specialized functions of the sclera are the drainage of aqueous humor and the mechanical support provided for the fibers of the optic nerve during their passage through the eye wall. Drainage of aqueous humor from the anterior chamber is controlled partly by a specialized part of the sclera, the trabecular meshwork, and partly by the uveoscleral route of which the final segment involves passive transscleral fluid transport. The lamina cribrosa is the specialized part of the sclera that provides mechanical support for the optic nerve as it leaves the eye. Disturbances in the biochemistry and biomechanical properties of the sclera can have severe consequences for the visual function by producing an eye that is not spherical, too long, too short, too rigid, or too elastic. Such disturbances can also interfere with the vascular supply of the eye, the control mechanisms of the intraocular pressure, or the resistance of the transscleral volume flow.

      PubDate: 2017-12-12T09:30:58Z
  • List of contributors
    • Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 9

      PubDate: 2017-12-12T09:30:58Z
  • List of contributors
    • Abstract: Publication date: 2000
      Source:Advances in Organ Biology, Volume 8

      PubDate: 2017-12-12T09:30:58Z
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