Central v1 avp receptors are involved in cardiovascular adaptation
to hypovolemia in wky but not in shr rats.
Budzikowski, Adam, Piotr Paczwa, and Ewa Szczepaska-Sadowska.
Department of Clinical and Applied Physiology, Warsaw Medical
Academy, Poland
APStracts 3:0077H, 1996.
The present study was designed to determine the role of centrally
released arginine vasopressin (AVP) in cardiovascular adaptation to
hypotensive hypovolemia in conscious normotensive (WKY) and
spontaneously hypertensive (SHR) rats. Three groups of experiments
were performed on WKY and SHR rats chronically implanted with the
lateral cerebral ventricle (ICV) cannula and with the femoral artery
catheter. Mean arterial pressure (MAP) and heart rate (HR) were
monitored before and after arterial bleeding (1.3% body weight)
performed during ICV infusion of: 1) artificial CSF (control), 2) V1
AVP receptors antagonist [d(Et2)Tyr(Me)DAVP, 5ng/min] and, 3) V2 AVP
receptors antagonist [d(CH2)5[D-Ile2,Ile4, AlaNH2]AVP, 5ng/min]. In
control experiments hemorrhage caused similar significant decreases
of MAP in both strains and bradycardia in WKY. Blockade of central V1
AVP receptors abolished hemorrhagic bradycardia and significantly
reduced hypotension in WKY having no effect on HR and MAP responses
to hypovolemia in SHR. Neither in WKY nor in SHR were the
cardiovascular responses to hemorrhage altered by blockade of central
V2 receptors. The results suggest that central V1 AVP system plays a
significant role in eliciting hypovolemic bradycardia and hypotension
in WKY and that this function is significantly impaired in SHR.
Received 19 July 1995; accepted in final form 9 February 1996.
APS Manuscript Number H681-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96