ROLE OF VASOPRESSIN ON CARDIOVASCULAR CHANGES DURING HEMORRHAGE IN CONSCIOUS RATS

Hypotensive hemorrhage decreases heart rate (HR) and renal sympathetic nerve activity (RSNA). Hemorrhage is a potent stimulus for arginine v asopressin (AVP) release; therefore, AVP may contribute to such inhibi tory action of HR and RSNA during hemorrhage. We evaluated the roles o f vasopressin on the regulation of blood pressure (BP), HR, and RSNA d uring hemorrhage using nonpeptide and selective V-1- and V-2-receptor antagonists (OPC-21268 and OPC-31260) in conscious rats. After hemorrh age (20 ml/kg body wt) BP decreased by 62 +/- 10 mmHg along with brady cardia (-110 +/- 15 beats/min) and renal sympathoinhibition (-50 +/- 8 ). Pretreatment of V-1-receptor antagonist (5 mg/kg iv) did not affect the initial fall of BP but attenuated subsequent BP recovery. Bradyca rdic and renal sympathoinhibitory responses following hemorrhage were abolished (-14 +/- 24 beats/min and -7 +/- 9) by V-1-receptor antagoni st. Pretreatment of V-2-receptor antagonist (1 mg/kg iv) did not affec t the response of BP; however, it did slightly strengthen bradycardia and prolong renal sympathoinhibition. Hemorrhage increased the plasma AVP concentration more than 50-fold. These results indicate that when the plasma concentration of AVP is extremely high during hemorrhage, v asopressin via V-1 receptor contributes to BP recovery by the peripher al vasoconstriction and exerts an inhibitory action on RSNA, and vasop ressin via V-2 receptor exerts opposite stimulatory action on RSNA.