Renal medullary circulation: Hormonal control

Chou, Shyan–Yih; Porush, Jerome G.; Faubert, Pierre F.

doi:10.1038/ki.1990.1

Cited by 107 publications

(58 citation statements)

References 76 publications

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“…10 ' 11 Alternatively, L-NA treatment could have altered tubular transport by decreasing renal medullary blood flow, which may indirectly influence tubular sodium and water transport by reducing renal interstitial fluid pressure 9 or by altering the renal cortical-medullary solute gradient. 12 Because there were no significant effects on glomerular filtration rate, fractional sodium or water excretion, or urine osmolality in the present study, it is difficult to determine the mechanism of the sodium and water retention.…”

Section: Discussionmentioning

confidence: 65%

Role of nitric oxide in renal papillary blood flow and sodium excretion.

1992

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Renal medullary interstitial infusion of A^'-nitro-L-arginine (120 fig/hr, n=7) decreased papillary blood flow to 71 ±5% of control without altering outer cortical flow. Before A' G -nitro-L-arginine infusion, interstitial acetylcholine administration (200 jtg/hr) increased cortical and papillary blood flow to 134±6% and 113±2% of control, respectively. After JV G -nitro-L-arginine administration, the vasodilator response to acetylcholine was abolished. In clearance experiments, renal medullary infusion of A' G -nitro-L-arginine (120 /tg/hr, n=l) significantly decreased total renal blood flow by 10%, renal interstitial fluid pressure by 23%, sodium excretion by 34%, and urine flow by 39% without altering glomerular filtration rate, fractional sodium and water excretion, blood pressure, or urine osmolality. These data indicate that selective inhibition of nitric oxide in the renal medullary vasculature reduces papillary blood flow, which is associated with decreased sodium and water excretion. We conclude that nitric oxide exerts a tonic influence on the renal medullary circulation. 7 These data suggest that the renal medulla produces NO, which may exert a paracrine influence on tubular or vascular function in this portion of the kidney.In the present studies, a nonpressor dose of the NO inhibitor JV G -nitro-L-arginine (L-NA) was infused directly into the renal medullary interstitium of anesthetized rats to determine if NO inhibition in the renal medulla would selectively reduce inner medullary blood flow. The effects of a selective reduction of inner medullary blood flow on renal interstitial fluid pressure and sodium and water excretion were then examined. Methods Surgical PreparationExperiments were performed on 24 male SpragueDawley rats purchased from SASCO, Inc., Madison, Wis.

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Section: Discussionmentioning

confidence: 65%

Role of nitric oxide in renal papillary blood flow and sodium excretion.

1992

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“…In contrast, blood fl ow in the outer medulla is less than 50 % of the cortical blood fl ow to preserve osmotic gradients and to enhance urinary concentration [10]. Th e combi nation of low me dullary perfusion, high oxygen consumption of the medullary thick ascending limbs (mTAL) and the countercurrent exchange of oxygen within the vasa recta, results in a poorly oxygenated outer medulla [11].…”

Section: Regional Intrarenal Oxygenation and Medullary Hypoxiamentioning

confidence: 99%

Renal Oxygenation in Clinical Acute Kidney Injury

Ricksten¹,

Bragadottir²,

Redfors³

2013

Annual Update in Intensive Care and Emergency Medicine 2013

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Renal oxygenation is defi ned as the relationship between renal oxygen delivery (DO 2 ) and renal oxygen consumption (VO 2 ) and it can easily be shown that the inverse of this relationship is equivalent to renal extraction of O 2 (O 2 Ex). An increase in renal O 2 Ex means that renal DO 2 has decreased in relation to renal VO 2 , i. e., renal oxygenation is impaired, and vice versa. When compared to other major organs, renal VO 2 is relatively high, second only to the heart. In sedated, mechanically ventilated patients, renal VO 2 is two-thirds (10 ml/min) that of myocardial oxygen consumption (15 ml/min) (Table 1) [1,2]. Renal blo od fl ow, w hich accounts for approximately 20 % of cardiac output, is three times higher than myocardial blood fl ow in this group of patients. Renal O 2 Ex in the non-failing kidney is therefore low, 10 %, compared with, e.g., the heart, in which O 2 E X is 55 % (Table 1). Determin a nts of renal oxygenationIt is well known from experimental studies that tubular sodium reabsorption is the major determinant of renal VO 2 [3] and tha t under normal physiological conditions, approximately 80 % is used to drive active tubular transport of particularly sodium, but also glucose, amino acids and other solutes. Tubular transport processes are highly load-dependent and it has been shown in experimental studies [4] and in p atients [2,[5][6][7] that the re i s a close linear correlation between glomerular fi ltration rate (GFR), renal sodium reabsorption and renal VO 2 (Fig. 1). Th e fi l tered load of sodium is, thus, an important determi nant of renal VO 2 and maneuvers that decrease GFR and the tubular sodium load act to decrease tubular sodium reabsorption and renal VO 2 , and vice versa [8]. It has b een shown that renal O 2 Ex remains stable over a wide range of renal blood fl ows, which means that changes in renal DO 2 , caused by changes in renal blood fl ow, are directly off set by changes in renal VO 2 [9], i. e., r enal VO 2 is fl ow-dependent. Th us, unlike other organs where increases in blood fl ow will improve oxygenation, increased renal blood fl ow augments GFR and the fi ltered load of sodium, which will increase renal VO 2 . Due to this fl ow-dependency of renal VO 2 , renal oxygenation will re main constant, as long as renal blood fl ow and GFR change in parallel. Regional intrarenal oxygenation and medullary hypoxiaTh e relatively high renal blood fl ow is directed preferentially to the cortex to optimize the fi ltration process and solute reabsorption. In contrast, blood fl ow in the outer medulla is less than 50 % of the cortical blood fl ow to preserve osmotic gradients and to enhance urinary concentration [10]. Th e combi nation of low me dullary perfusion, high oxygen consumption of the medullary thick ascending limbs (mTAL) and the countercurrent exchange of oxygen within the vasa recta, results in a poorly oxygenated outer medulla [11]. Oxygen av ailability is, therefore, low in the outer medulla, which has an oxygen tissue partial pressure (PO 2 ) of 10-20 mm Hg ...

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“…The authors proposed that this expansion induced the release of another mediator inhibiting renal tubular sodium transport 4,39 ; however, our experiments show that AVP increased sodium excretion even in the absence of any fluid load. (2) Prostaglandins are known to reduce sodium transport in the CD 40 and to increase medullary blood flow, 41,42 two effects that each will contribute in different ways to increased sodium excretion. Actually, prostaglandins have been shown to contribute to the AVP-induced natriuresis.…”

Section: V1ar Effectsmentioning

confidence: 99%

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Perucca

Bichet²,

Bardoux

et al. 2008

Journal of the American Society of Nephrology

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The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and pressor effects, via activation of V2 and V1a receptors, respectively, are relatively well understood, but the possible associated effects on sodium handling are a matter of controversy. In this study, normal conscious Wistar rats were acutely administered various doses of AVP, dDAVP (V2 agonist), furosemide, or the following selective non-peptide receptor antagonists SR121463A (V2 antagonist) or SR49059 (V1a antagonist). Urine flow and sodium excretion rates in the next 6 h were compared with basal values obtained on the previous day, after vehicle treatment, using each rat as its own control. The rate of sodium excretion decreased with V2 agonism and increased with V2 antagonism in a dose-dependent manner. However, for comparable increases in urine flow rate, the V2 antagonist induced a natriuresis 7-fold smaller than did furosemide. Vasopressin reduced sodium excretion at 1 g/kg but increased it at doses Ͼ5 g/kg, an effect that was abolished by the V1a antagonist. Combined V2 and V1a effects of endogenous vasopressin can be predicted to vary largely according to the respective levels of vasopressin in plasma, renal medulla (acting on interstitial cells), and urine (acting on V1a luminal receptors). In the usual range of regulation, antidiuretic effects of vasopressin may be associated with variable sodium retention. Although V2 antagonists are predominantly aquaretic, their possible effects on sodium excretion should not be neglected. In view of their proposed use in several human disorders, the respective influence of selective (V2) or mixed (V1a/V2) receptor antagonists on sodium handling in humans needs reevaluation. 19: 172119: -173119: , 200819: . doi: 10.1681 The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and its pressor effects are relatively well understood. On the one hand, AVP improves water conservation by increasing the permeability to water of the renal collecting duct (CD), an effect mediated by the V2 receptors (V2R) and permitted by the insertion in the luminal membrane of principal cells of preformed aquaporin 2 (AQP2) molecules. This allows more water to be reabsorbed when these ducts traverse the hyperosmotic medulla. On the other hand, AVP increases blood pressure (BP) by inducing a vasoconstriction through its binding to V1a receptors (V1aR) expressed in vascular smooth muscle cells. For these two different effects, in vivo studies are in good agreement with the expectations based on results obtained in vitro. J Am Soc NephrolIn contrast, the experiments intended to study the effects of AVP on sodium handling in vitro or in vivo provide results that are difficult to reconcile. In the isolated microperfused CD, V2R activation increases sodium transport, 1 an effect that should reduce sodium excretion in vivo; however, in a number of studies, AVP infusion in animals and humans

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Renal medullary circulation: Hormonal control

Cited by 107 publications

References 76 publications

Role of nitric oxide in renal papillary blood flow and sodium excretion.

Role of nitric oxide in renal papillary blood flow and sodium excretion.

Renal Oxygenation in Clinical Acute Kidney Injury

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

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