CENTRAL V-1 AVP RECEPTORS ARE INVOLVED IN CARDIOVASCULAR ADAPTATION TO HYPOVOLEMIA IN WKY BUT NOT IN SHR

The present study was designed to determine the role of centrally rele ased arginine vasopressin (AVP) in cardiovascular adaptation to hypote nsive hypovolemia in conscious normotensive Wistar-Kyoto rats (WKY) an d spontaneously hypertensive rats (SHR). Three groups of experiments w ere performed on WKY and SHR chronically implanted with lateral cerebr al ventricle (LCV) cannulas and with femoral artery catheters. Mean ar terial pressure (MAP) and heart rate (HR) were monitored before and af ter arterial bleeding (1.3% body weight) performed during LCV infusion of 1) artificial cerebrospinal fluid (control), 2) V-1 AVP-receptor a ntagonists {[d(Et(2))Tyr(Me)]DAVP, 5 ng/min}, and 3) V-2 AVP-receptor antagonists {[d(CH2)(5)-D-Ile(2),Ile(4), AlaNH(2)]AVP, 5 ng/min}. In c ontrol experiments hemorrhage caused similar significant decreases of MAP in both strains and bradycardia in WKY. Blockade of central V-1 AV P-receptors abolished hemorrhagic bradycardia and significantly reduce d hypotension in WKY, with no effect on HR and MAP responses to hypovo lemia in SHR. Neither in WKY nor in SHR were the cardiovascular respon ses to hemorrhage altered by blockade of central V-2 receptors. The re sults suggest that the central V-1 AVP system plays a significant role in eliciting hypovolemic bradycardia and hypotension in WKY and that this function is significantly impaired in SHR.