AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 2 431-R438, Copyright © 1989 by American Physiological Society
Alternative mechanism for attenuated pressor responses in AV3V-lesioned dogs
A. F. Tramposch, O. U. Lopes, C. L. Chernicky and C. M. Ferrario
Department of Brain and Vascular Research, Cleveland Clinic Foundation, Ohio 44195.
We lesioned the periventricular tissue of the anteroventral portion of the
third cerebral ventricle (AV3V) of dogs to evaluate the mechanism that
accounts for blunting of the pressor activity of angiotensin II (ANG II).
AV3V lesions were done with a microknife using a transbuccal approach; the
procedure denervated the organum vasculosum of the laminae terminalis, the
nucleus medianus, and the medial preoptic nucleus. Two to four days after
surgery, the conscious AV3V-lesioned dogs showed adipsia and their blood
contained increased quantities of Na+ (175 +/- 2 meq/l) and an elevated
osmolality (352 +/- 5 mosmol/kg). Cardiac rate was faster (131 +/- 8
beats/min) in AV3V-lesioned dogs, but their mean arterial pressure (MAP)
was within normal values (99 +/- 4 mmHg). These changes were accompanied by
an almost 18-fold increase in the plasma levels of immunoreactive ANG II
(irANG II). In contrast, plasma vasopressin (AVP) levels fell to
nondetectable values. Pressor responses produced by intravenous infusions
of ANG II or injections of norepinephrine (NE) were significantly blunted 3
days after AV3V ablation. Short-term treatment of eight AV3V-lesioned dogs
with the synthetic AVP analogue, 1-desamino-8-D-arginine vasopressin,
reduced plasma Na+ and irANG II levels. The pressor activity of peripheral
infusions of ANG II was restored to prelesion values, whereas pressor
responsiveness to NE remained depressed. These data suggest that the
blunting of the pressor action of ANG II in AV3V-lesioned dogs is an
expression of a disorder in the regulation of renal and behavioral
mechanisms maintaining fluid balance and AVP secretion.(ABSTRACT TRUNCATED
AT 250 WORDS)
