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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

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