AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 3 838-R849, Copyright © 1994 by American Physiological Society
Vasopressin-induced changes in cardiac vagal tone and oxygen consumption in dogs
J. F. Liard
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
Experiments were conducted in 63 dogs to determine whether stimulation of
vagal tone contributes to the decrease in O2 consumption (VO2) that results
from arginine vasopressin (AVP) administration. Vagal stimulation with
pilocarpine did not reduce VO2 in conscious dogs. In anesthetized dogs,
bilateral electrical cervical efferent vagal stimulation lowered both
cardiac output (CO; by 46%) and VO2 (by 22%) over the first 5 min. Between
7 and 11 min of stimulation, CO remained decreased, but VO2 returned to
control. Significant increases in left atrial pressure, bradycardia, and a
fall in mean arterial pressure accompanied vagal stimulation. All these
effects of cervical vagal stimulation were abolished by cardiac denervation
and also by pacing. Administration of a selective AVP V1 agonist led to
significant reductions of CO and VO2. Cardiac denervation prevented the
decrease in VO2 induced by AVP infusion, but not the decrease in CO. During
AVP infusions, pacing at a rate slightly higher than control heart rate did
not prevent the fall in CO or in VO2, whereas pacing at 150 beats/min
prevented part of the fall in VO2. Sinoaortic denervation or atropine
treatment prevented the decrease in VO2 resulting from AVP infusion. The
combination of alpha- and beta-blockade did not affect the CO or the VO2
response to AVP infusion, nor did naloxone treatment. The administration of
atrial or ventricular extracts, but not that of alpha-human atrial
natriuretic peptide, led to a significant reduction in VO2. These results
are compatible with the hypothesis that AVP infusion increases vagal tone
to the heart, which, possibly as a result of increased left atrial pressure
and reduced heart rate, may release a factor reducing VO2.
