AJP - Heart and Circulatory Physiology, Vol 247, Issue 3 349-H360, Copyright © 1984 by American Physiological Society
Central nervous system action of angiotensin during onset of renal hypertension in awake rats
J. E. Faber and M. J. Brody
The increase in arterial pressure and vascular resistance during acute
unilateral renal artery stenosis (RSt) in conscious rats is, in part,
dependent on elevated neurogenic vascular tone produced by an indirect
neural interaction of angiotensin II (ANG II) with the sympathetic nervous
system. The present experiments examined whether this interaction occurs
within the central nervous system. Conscious rats that had been chronically
instrumented with miniaturized Doppler flow probes for measurement of
regional vascular resistance were subjected to a 50% reduction in
unilateral renal flow with an implanted pneumatic occluder. Arterial
pressure increased by 35% after 60 min of RSt. In animals in which the
pressor response to intracerebroventricular (icv) ANG II had been
eliminated by prior surgical interruption of the "ANG II pressor pathway"
in the anterior hypothalamus, the increase in blood pressure following RSt
was attenuated by 44% (P less than 0.01). In a second series, a central
action of ANG II during acute renal hypertension (RH) was assessed by
central ANG II receptor blockade with icv saralasin. Unlike normotensive
controls, acutely RH animals responded to saralasin with significant (P
less than 0.01) decreases in arterial pressure (-32%) and hindquarters
(-26%) and contralateral renal (-9%) resistance. These changes were
accentuated (-57% decrease in pressure) in animals made areflexic by prior
sinoaortic baroreceptor denervation. Thus activation of the sympathetic
nervous system during the early high-renin phase of RH depends
significantly on a central action of ANG II. This mechanism may account for
some 40-50% of the pressure increase following acute RSt.
