During acute hypercapnia vasopressin inhibits an angiotensin drive to ventilation in conscious dogs. Walker, Julia K. L., and Donald B. Jennings. Department of Physiology, Queen's University, Kingston, Ontario CANADA K7L 3N6
APStracts 2:0184A, 1995.
Intravenous infusion of vasopressin (AVP) depresses the slope of the ventilatory response to CO2 (VRC) during acute hypercapnia. We therefore tested the hypothesis that AVP V1 receptor block would increase the slope of the VRC. Following a 20 min control period, an AVP V1 receptor antagonist (d(CH2)5[Tyr(Me)2]AVP) was injected into 6 conscious resting dogs. Thirty minutes following AVP V1 receptor block dogs were exposed to sequential 20 minute periods of 5% and 6.5% inspired CO2 in air. A second protocol (no AVP V1 receptor block) was conducted as a control. As predicted, AVP V1 receptor block enhanced ventilation during inhalation of 6.5% CO2, in association with an increased metabolic rate and increased plasma angiotensin II (ANG II). In eupneic dogs, stimulation of respiration by AVP V1 receptor block is mediated by ANG II. A third protocol with ANG II receptor block (intravenous infusion of saralasin) combined with AVP V1 receptor block indicated that ANG II mediated the increase in metabolism and the augmented ventilation during inhalation of 6.5% CO2. We conclude that during acute hypercapnia of sufficient magnitude, and perhaps duration, AVP inhibits an ANG II mediated stimulation of metabolism and respiration. 

Received 27 May 1994; accepted in final form 25 April 1995.
APS Manuscript Number A520-4.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  9 May 1995.