Arginine vasopressin-induced natriuresis in the anaesthetized rat: involvement of V1 and V2 receptors

Abstract

ABSTRACT The present study was undertaken to determine the involvement of the two established vasopressin receptor subtypes (V1 and V2) in arginine vasopressin (AVP)-induced natriuresis and also to determine whether changes in mean arterial pressure (MAP) and/or the renally active hormones atrial natriuretic peptide (ANP), angiotensin II (AII) and aldosterone are a prerequisite for the expression of AVP-induced natriuresis. In Sprague–Dawley rats which were anaesthetized with Inactin (5-ethyl-5-(1′-methylpropyl)-2-thiobarbiturate) and infused with 0·077 mol NaCl/l, infusion of 63 fmol AVP/min was found to be natriuretic whereas an approximately equipotent dose of the specific V2 agonist [deamino-cis1, d-Arg8]-vasopressin (dDAVP) did not induce natriuresis. The specific V1 antagonist [β-mercapto-β,β-cyclopenta-methylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin when administered prior to infusion of 63 fmol AVP/min did not inhibit AVP-induced natriuresis. AVP-induced natriuresis was not accompanied by changes in MAP or in the plasma concentrations of the renally active hormones ANP, AII or aldosterone. These results suggest that neither the V1 nor the V2 receptor subtypes are involved in AVP-induced natriuresis. In addition, it was found that changes in MAP, plasma ANP, All or aldosterone concentrations were not a prerequisite for AVP-induced natriuresis. Journal of Endocrinology (1993) 136, 283–288