Baroreflex buffering of pressor response to vasopressin is mediated by V1, not V2, receptors in conscious rats
Shimizu, K.; Schwartz, J.; McGrath, B.P.
American Journal of Physiology 264(2 Pt 2): R345-R349
1993
ISSN/ISBN: 0002-9513 PMID: 8447490 Document Number: 417041
Arginine vasopressin (AVP) enhances reflex buffering of its own pressor response, thus attenuating its vasoconstrictor potential in vivo. To investigate the extent to which this effect of AVP is mediated by V-1 or V-2 receptors, mean arterial pressure (MAP) and heart rate (HR) changes were examined in response to graded injections of AVP or (Phe-2,Orn-8)oxytocin, a potent, selective V-1-receptor agonist, in the absence and presence of infusion of (Val-4,D-Arg-8)VP, a selective V-2-receptor agonist. Responses were compared in intact and autonomically blocked conscious rats. During autonomic blockade with methscopolamine and hexamethonium, the pressor sensitivities to AVP and (Phe-2,Orn-8)oxytocin were similarly increased. Infusion of the V-2-receptor agonist had no effect by itself on MAP or HR in conscious intact rats. It also did not alter the pressor responses to the V-1 agonist, in either intact or autonomically blocked rats. In the presence of the V-2 agonist, the decrease in heart rate induced by the V-1 agonist was enhanced. These results indicate that reflex buffering of the pressor response to AVP in the conscious rat is mediated by V-1 and not V-2 receptors. However, V-2 receptors may be involved in modulating the heart rate response to AVP.