AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 3 476-R480, Copyright © 1986 by American Physiological Society
Activation of the central vasopressin system: a common pathway for several centrally acting pressor agents
K. A. Gruber and S. L. Eskridge
Hypertonic saline (HS) and angiotensin II (ANG II) administered centrally
or peripherally produce a forebrain-mediated central nervous system-(CNS)
dependent pressor action. Although the majority of these effects are due to
increased central sympathetic drive and inhibition of the cardiac
baroreceptor reflex, evidence from peripheral infusions of vasopressin (Vp)
receptor antagonists have suggested that part of the blood pressure
increase may be due to circulating Vp. We now report that blockade of CNS
Vp receptors in rats, via a fourth ventricle infusion of a Vp receptor
antagonist, attenuated greater than 70% of the pressor response to lateral
ventricle infusion of HS, ANG II, or hypertonic glucose (HG). Intravenous
administration of the Vp antagonist could block only 40% of the HS
response. When lateral ventricle infusion of HS was performed in rats with
a hereditary lack of Vp (diabetes insipidic rats) no pressor response was
obtained. Because centrally administered Vp has autonomic nervous system
effects that are similar to those induced by HS or ANG II, our results
suggest that CNS Vp may provide a link between forebrain acting pressor
agents and autonomic nervous system regulation. Finally, HG produced a
pressor effect that had an equivalent peak response to HS. However, unlike
the HS response, the pressor effect to HG returned to base line within
approximately 5 min during a 10-min infusion. Thus there appears to be a
quantitative difference in the pressor responses produced by activation of
sodium vs. osmoreceptors.
