AJP - Heart and Circulatory Physiology, Vol 253, Issue 6 1523-H1529, Copyright © 1987 by American Physiological Society
Renal vascular reactivity to U 46619 and adrenergic agonists in Goldblatt hypertension
B. G. Zimmerman
Department of Pharmacology, University of Minnesota, Minneapolis 55455.
Vascular reactivity of the contralateral kidney of conscious Goldblatt
hypertensive dogs was studied by eliciting renal blood flow (RBF) responses
to intra-arterial infusions of vasoconstrictor and vasodilator agonists in
control sessions and at weekly intervals postclipping. Systemic arterial
blood pressure (BP) and RBF were monitored during each recording session
via an implanted catheter and electromagnetic blood flow probe,
respectively. BP was maximally increased within 1 wk and remained elevated
for the duration of the study. The relationship between the negative
percent change in RBF (-% delta RBF) and the renal arterial plasma
concentration of adrenergic agonists, angiotensin II and thromboxane
mimetic (U 46619), infused intra-arterially was subjected to regression
analysis, and 25 and 50% effective doses (ED25 and ED50, respectively) were
calculated. Vascular sensitivity to phenylephrine and norepinephrine
increased within a month or more of hypertension. Vascular reactivity to
angiotensin II was unchanged. In contrast to the delayed increase in renal
vascular reactivity to adrenergic agonists, enhancement of the RBF
responses to U 46619 was seen within 1-2 wk. In addition,
beta-adrenoceptor-mediated vasodilation appeared suppressed during
hypertension. Alteration in the response of the contralateral kidney to
both vasoconstrictor and beta-adrenoceptor-mediated vasodilator stimuli may
contribute to renal hemodynamic changes in Goldblatt hypertension.
