AJP - Heart and Circulatory Physiology, Vol 252, Issue 6 1243-H1248, Copyright © 1987 by American Physiological Society
Postpropranolol vasodilation in adrenalectomized glucocorticoid hypertensive rats
D. J. DiPette, J. F. Burris, A. Rogers, B. Waeber and H. R. Brunner
Acute beta-adrenoreceptor blockade results in an enhanced blood
pressure-lowering effect in glucocorticoid hypertensive rats in the absence
of the adrenals. To evaluate the possible mechanism of this enhanced blood
pressure-lowering effect, systemic and regional hemodynamics were
determined by the radioactive microsphere technique before and after
propranolol administration in bilaterally adrenalectomized (AX) and
sham-operated (SH) glucocorticoid hypertensive rats. Propranolol decreased
mean blood pressure (BP) and heart rate (HR) to a greater extent in the AX
animals. In response to propranolol, cardiac output (CO) decreased equally
in both the AX and SH animals. Regional vascular responses to propranolol
were similar between the AX and SH animals, except in muscle. In muscle
propranolol significantly decreased blood flow and increased resistance in
the SH animals. In marked contrast, in the AX animals propranolol
significantly increased blood flow and decreased vascular resistance. The
results of this study show that in adrenalectomized glucocorticoid
hypertensive rats, the enhanced BP lowering effect of acute
beta-adrenoreceptor blockade is not mediated by changes in CO.
Additionally, in glucocorticoid hypertensive rats acute beta-adrenoreceptor
blockade causes selective vasodilation in skeletal muscle.
