Respiration during acute hypoxia and hypoxic hypercapnia:
angiotensin ii and vasopressin v1 receptor block.
Overgaard, Christopher B., Julia K. L. Walker, and Donald B. Jennings.
Department of Physiology, Queen's University, Kingston, Ontario,
Canada, K7L 3N6
APStracts 2:0488A, 1995.
In normoxic conscious dogs, increased angiotensin II (ANG II), or
activation (disinhibition) of the renin-angiotensin system by
vasopressin (AVP) V1 receptor block, increases ventilation and
decreases PaCO2. Both hormones can be increased during hypoxia and
might modulate ventilatory drive. Six conscious dogs were studied
prior to, and during hypocapnic, isocapnic and hypercapnic hypoxia.
To study potential hormonal effects during hypocapnic hypoxia,
Experiment 1 included three protocols in which 12.8% O2 was breathed
for 60 min: Protocol 1) control studies without block, Protocol 2)
AVP V1 receptors were blocked at the onset of hypoxia, and Protocol
3) ANG II receptors were blocked 20 min prior to hypoxia. To study
potential effects of acid-base changes during acute hypoxia,
Experiment 2 included two protocols (with and without AVP V1 receptor
block). A 40 min period of hypocapnic hypoxia was followed by two
successive 20 min periods with hypoxia maintained but inspired CO2
progressively increased. Neither hormonal block affected respiration
during the hypoxic conditions. Unlike normoxia in conscious dogs,
during acute hypoxia respiratory control by ANG II is not modulated
by AVP, and acid-base effects on receptors do not account for this
difference.
Received 21 June 1995; accepted in final form 30 October 1995.
APS Manuscript Number A665-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95