AJP - Heart and Circulatory Physiology, Vol 247, Issue 6 991-H998, Copyright © 1984 by American Physiological Society
Hemodynamic and neural mechanisms of acute neurogenic hypertension in the rat
A. H. Werber, W. J. Bryan and G. D. Fink
Experiments were performed to test the hypothesis that acute hypertension
caused by aortic baroreceptor deafferentation (ABD) is the result of
sympathetic vasoconstriction. Cardiac output (CO), mean arterial pressure
(MAP), and total peripheral resistance (TPR) were measured before and after
ABD in anesthetized and conscious rats. The role of the sympathetic nervous
system in acute ABD-induced hypertension was evaluated by examining the
ability of adrenalectomy, adrenal demedullation, guanethidine or combined
adrenal demedullation, and guanethidine pretreatment to prevent, and total
autonomic blockade to reverse, ABD-induced hypertension. CO did not change
significantly after ABD at any time, whereas MAP and TPR increased
significantly (P less than 0.05). Only combined adrenal demedullation and
guanethidine pretreatment prevented ABD-induced hypertension, and autonomic
blockade normalized MAP in ABD rats. Normalization of blood pressure was
the result of a decreased TPR. It is concluded that acute ABD-induced
hypertension results from vasoconstriction caused by neurally released
and/or circulating catecholamines.
