Interaction between V1 and V2 effects in hemodynamic response to vasopressin in dogs.

We investigated in conscious, chronically instrumented dogs whether actions mediated by V1 receptors affect cardiovascular effects elicited by V2-like receptors in response to vasopressin or vasopressin analogues. Infused arginine vasopressin (AVP) (220 pg.kg-1.min-1) did not have any significant effect on arterial pressure, cardiac output (CO), and heart rate (HR) when it was preceded by administration of a V1 receptor antagonist. However, when the same antagonist was administered 1 h after the start of the same infusion of AVP, CO, and HR increased significantly above control pre-AVP values, and total peripheral resistance (TPR) fell significantly below control. When a combined V1+V2 receptor antagonist was administered after 1 h of AVP infusion at the same rate, CO, HR, and TPR returned to, but not beyond, control values. When a selective V1 agonist was infused for 1 h, the administration of a V1 antagonist also returned hemodynamic values to, but not beyond, control. These results suggest that 1-h administration of AVP sensitized V2-like receptors to moderate levels of circulating AVP. In another set of experiments, the administration of a selective V1 agonist blunted significantly the CO and HR increase as well as the decrease in TPR normally associated with injection of a selective V2 agonist. However, administration of phenylephrine did not reduce these V2-mediated effects. We conclude that there are significant interactions between V1 and V2-like receptors in the cardiovascular system of conscious dogs, whereby V1 effects appear to 1) immediately antagonize the action of V2 agonists and 2) sensitize the organism to cardiovascular effects mediated by V2-like receptors after a prolonged exposure.(ABSTRACT TRUNCATED AT 250 WORDS)