AJP - Regulatory, Integrative and Comparative Physiology, Vol 262, Issue 4 636-R643, Copyright © 1992 by American Physiological Society
V1- and V2-receptor contributions to ovine fetal renal and cardiovascular responses to vasopressin
M. G. Ervin, M. G. Ross, R. D. Leake and D. A. Fisher
Department of Obstetrics and Gynecology, University of California, Los Angeles, School of Medicine, Torrance 90502.
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.
