Postpropranolol vasodilation in adrenalectomized glucocorticoid hypertensive rats.
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.
D000315:Adrenalectomy; D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D005938:Glucocorticoids; D006339:Heart Rate / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008863:Microspheres; D011433:Propranolol / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects*
D005938:Glucocorticoids; D011433:Propranolol