Pericyte Regulation of Renal Medullary Blood Flow

Pallone, Thomas L.; Silldorff, Erik P.

doi:10.1159/000052608

Cited by 124 publications

(104 citation statements)

References 14 publications

(19 reference statements)

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“…The classic depiction of vasa recta as passive filters that provide countercurrent exchange and solute trapping belies the complexity of their structure and function. DVR are arterioles that respond to an array of vasoactive agents (111). They are also transporting microvessels that express specific transporters for water (AQP1) and urea (UTB) (92,93,168).…”

Section: Discussionmentioning

confidence: 99%

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Physiology of the renal medullary microcirculation

Pallone

Zhang

Rhinehart

2003

American Journal of Physiology-Renal Physiology

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186

193

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Pallone, Thomas L., Zhong Zhang, and Kristie Rhinehart. Physiology of the renal medullary microcirculation. Am J Physiol Renal Physiol 284: F253-F266, 2003; 10.1152/ajprenal.00304.2002.-Perfusion of the renal medulla plays an important role in salt and water balance. Pericytes are smooth muscle-like cells that impart contractile function to descending vasa recta (DVR), the arteriolar segments that supply the medulla with blood flow. DVR contraction by ANG II is mediated by depolarization resulting from an increase in plasma membrane Cl Ϫ conductance that secondarily gates voltage-activated Ca 2ϩ entry. In this respect, DVR may differ from other parts of the efferent microcirculation of the kidney. Elevation of extracellular K ϩ constricts DVR to a lesser degree than ANG II or endothelin-1, implying that other events, in addition to membrane depolarization, are needed to maximize vasoconstriction. DVR endothelial cytoplasmic Ca 2ϩ is increased by bradykinin, a response that is inhibited by ANG II. ANG II inhibition of endothelial Ca 2ϩ signaling might serve to regulate the site of origin of vasodilatory paracrine agents generated in the vicinity of outer medullary vascular bundles. In the hydropenic kidney, DVR plasma equilibrates with the interstitium both by diffusion and through water efflux across aquaporin-1. That process is predicted to optimize urinary concentration by lowering blood flow to the inner medulla. To optimize urea trapping, DVR endothelia express the UT-B facilitated urea transporter. These and other features show that vasa recta have physiological mechanisms specific to their role in the renal medulla. vasa recta; perfusion; hypertension; oxygenation; urinary concentration; patch clamp; calcium; fura 2 THE MICROCIRCULATION OF THE kidney is regionally specialized. In the cortex, afferent and efferent arterioles govern the driving forces that promote glomerular filtration. A dense peritubular capillary plexus arising from efferent arterioles surrounds the proximal and distal convoluted tubules to accommodate enormous reabsorption of glomerular filtrate. In contrast, vasa recta serve needs specific to the medulla. Through the counterflow arrangement of descending (DVR) and ascending vasa recta (AVR), countercurrent exchange traps NaCl and urea deposited to the interstitium by collecting ducts and the loops of Henle. This is vital to maintain corticomedullary osmotic gradients but conflicts with the need to supply nutrient blood flow to medullary tissue. Metabolic substrates that enter the medulla in DVR blood diffuse to the AVR to be shunted back to the cortex. To deal with the threat of medullary hypoxia resulting from this process, the kidney has evolved a capacity to exert subtle control over regional perfusion of the outer and inner medulla. The details are far from clear, but much experimental evidence points to the complex interactions of many autocoids and paracrine agents to modulate vasomotor tone at various sites along the microvascular circuit. The goal of this review is to summarize ...

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Section: Discussionmentioning

confidence: 99%

“…The DVR wall is characterized by smooth muscle remnants that surround a continuous endothelium and impart contractile function. The pericytes persist into the inner medulla but eventually disappear (111,120). Near their termination, DVR become fenestrated and give rise to a sparse capillary plexus.…”

Section: Renal Medullary Microvascular Anatomymentioning

confidence: 99%

Physiology of the renal medullary microcirculation

Pallone

Zhang

Rhinehart

2003

American Journal of Physiology-Renal Physiology

Self Cite

186

193

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“…81 They play a critical role in the stability and integrity of microvessels and are able to control microcirculation by regulating capillary diameter and hence vascular tone. 81,82 In response to injury, pericytes detach, migrate to the interstitial space and transform into myofibroblasts (Figure 2). Pericytes transformation has been demonstrated in experimental models of UUO and IR .…”

Section: Renal Inflammation and Fibrosis: The Kidney's Response To Inmentioning

confidence: 99%

Current Understanding of the Pathogenesis of Progressive Chronic Kidney Disease in Cats

Jepson

2016

Veterinary Clinics of North America: Small Animal Practice

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Abstract:In cats with chronic kidney disease (CKD), the most common histopathological finding is tubulointerstitial inflammation and fibrosis. However, these changes reflect a non-specific response of the kidney to any inciting injury. The risk of development of CKD in a patient is likely to reflect genetic predispositions, ageing, environmental and individual factors that influence decline in renal function over the course of a cat's life. However, there is still relatively little information about exactly which risk factors predispose a cat to develop CKD and these will be explored. Whilst many cats diagnosed with CKD have stable disease for many years, some cats show overtly progressive disease.

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“…Vascular smooth muscle cells (including pericytes) around these descending vasa recta have vasoconstrictive properties (40). Thus tonic modulation of afferent and efferent arterioles and the descending vasa recta contributes to the regulation of renal O 2 supply and medullary blood flow, respectively.…”

Section: Microvascular Dysfunction and The Balance Between Vasoconstrmentioning

confidence: 99%

“…Although the mechanism behind this dysfunction remains unclear and various contributing factors have been suggested, the nitric oxide (NO) pathway is thought to be a main player (42,43). NO is well known for its role in vascular tone regulation by acting on vascular smooth muscle cells to induce vasodilation (40,44). NO is generated by the enzymatic transformation of L-arginine and O 2 into L-citrulline and NO; this reaction is catalyzed by an enzyme called nitric oxide synthase (NOS), which exists in three different isoforms, all of which are found in the kidney (42,45).…”

Section: Microvascular Dysfunction and The Balance Between Vasoconstrmentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

237

169

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Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

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Pericyte Regulation of Renal Medullary Blood Flow

Cited by 124 publications

References 14 publications

Physiology of the renal medullary microcirculation

Physiology of the renal medullary microcirculation

Current Understanding of the Pathogenesis of Progressive Chronic Kidney Disease in Cats

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

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