Role of Urinary Arginine Vasopressin in the Sodium Excretion in Patients With Chronic Renal Failure

Nonoguchi, Hiroshi; Takayama, M.; Owada, Akira; Ujiie, Kazutomo; Yamada, Takehisa; Nakashima, Osamu; Sakuma, Yoriko; Koike, Jun; Terada, Yoshio; Marumo, Fumiaki; Tomita, Kimio

doi:10.1016/s0002-9629(15)41815-4

Cited by 14 publications

(11 citation statements)

References 38 publications

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“…These findings suggest that the V1a receptor plays a role in maintaining minimal urine flow for renal function by acting against V2 receptor-mediated antidiuresis under chronically dehydrated conditions and that water and electrolyte metabo-lism may be controlled by the elaborate interaction between V1a and V2 receptors along the nephron. Urinary AVP serves as an intrinsic diuretic by inhibiting V2 receptormediated antidiuretic action via activating the V1a receptor (375,376).…”

Section: B Renal Functionmentioning

confidence: 99%

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

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332

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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Section: B Renal Functionmentioning

confidence: 99%

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

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332

297

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“…54 -57 (3) In patients with chronic renal failure, the increased urinary excretion of AVP per remaining nephron correlated positively and more significantly than for any other hormone with the fractional excretion of sodium, suggesting that luminal AVP contributed to ensure an appropriate natriuresis through V1aR-mediated luminal effects. 58 (4) Interestingly, mice with deletion of the V1aR exhibit a lower BP as a result not of a reduced vasoconstriction but of a lower extracellular fluid volume. 59 In summary, these results provide a better knowledge of the respective V2R-and V1aR-dependent effects of AVP on sodium excretion in rats.…”

Section: Integration Of V2r and 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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“…This pathway, at high-AVP concentrations, is expected to inhibit the Na ϩ /H ϩ exchanger (6). However, in recent years V 1 receptors have been detected in both apical and basolateral membrane domains and have been shown to mediate AVP activity via phospholipase C-inositol 3,4,5-triphosphate (IP 3 )-calcium signaling (14,15,23). On the other hand, it is known that protein kinase C, via phosphorylation, may stimulate the Na ϩ /H ϩ exchanger (11).…”

mentioning

confidence: 99%

Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V₁ and V₂receptors

Musa‐Aziz¹,

Barreto-Chaves

Mello-Aires³

2002

American Journal of Physiology-Renal Physiology

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Role of Urinary Arginine Vasopressin in the Sodium Excretion in Patients With Chronic Renal Failure

Cited by 14 publications

References 38 publications

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V₁ and V₂receptors

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Role of Urinary Arginine Vasopressin in the Sodium Excretion in Patients With Chronic Renal Failure

Cited by 14 publications

References 38 publications

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V1 and V2receptors

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Peritubular AVP regulates bicarbonate reabsorption in cortical distal tubule via V₁ and V₂receptors