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  • Title: V1- and V2-receptor contributions to ovine fetal renal and cardiovascular responses to vasopressin.
    Author: Ervin MG, Ross MG, Leake RD, Fisher DA.
    Journal: Am J Physiol; 1992 Apr; 262(4 Pt 2):R636-43. PubMed ID: 1566929.
    Abstract:
    To assess the contributions of arginine vasopressin (AVP) V1- and V2-receptors to the ovine fetal responses to AVP, we studied V2-receptor stimulation in the presence of V1-receptor blockade, and selective V2-receptor stimulation in chronically catheterized fetal lambs. AVP administration (20 ng/kg) to the saline infused fetuses (n = 8; 132 +/- 2 days) significantly increased mean arterial pressure (MAP; 45 +/- 2 to 53 +/- 4 mmHg) and urine osmolality (Uosm; 134 +/- 13 to 379 +/- 42 mosmol/kgH2O) and decreased heart rate (HR; 168 +/- 3 to 147 +/- 5 beats/min) and urine flow (V; 0.48 +/- 0.10 to 0.19 +/- 0.03 ml/min). V1-receptor antagonist infusion, [d(CH2)5,Tyr(Me)]AVP (n = 7; 134 +/- 1 days) had no effect on fetal MAP, Uosm, HR, or V. V1-receptor blockade abolished the MAP response to AVP without affecting the HR and urinary responses. In a second series of animals (n = 6; 131 +/- 1 days), selective V2-receptor agonist infusion [desmopressin (DDAVP)] had no effect on fetal MAP or HR while initial changes in V and Uosm were identical to the effects of AVP alone. Our results demonstrate clear discrimination of V1- and V2-receptor-mediated events in the fetal MAP and renal responses to AVP. Moreover, the HR response to AVP is not mediated by the population of V1-receptors blocked by [d(CH2)5,Tyr(Me)]AVP or V2-receptors stimulated by DDAVP, suggesting the presence of additional AVP receptor subclass(es) during fetal life.
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