Beta-adrenoceptor blockade and vasodilatation in essential hypertension. Hemodynamic studies at rest and during exposure to stress.

Abstract

The purpose of this study was to evaluate the acute and long-term effects on blood pressure and hemodynamics both at rest and during acute exposure to loud noise of drugs with beta-adrenoceptor blocking and vasodilating properties. Prizidilol and carvedilol both act as nonselective beta-blocking and precapillary vasodilating compounds. Prizidilol (200 mg X 2) was compared to propranolol (80 mg X 2) plus hydralazine (25 mg X 2) and showed similar antihypertensive effect in a long-term double-blind randomized trial. Carvedilol was evaluated acutely with invasive (dye-dilution) and noninvasive (plethysmography) technique and showed an acute antihypertensive effect without causing a rise in TPR and with a decrease in regional resistance in the fore-arm. Acutely, carvedilol (25 mg and 50 mg) decreased blood pressure and regional resistance (50 mg) in contrast to propranolol (80 mg) which did not lower blood pressure acutely and caused an increase in regional resistance. In a long-term double-blind, randomized comparison, both propranolol (80 mg X 2) and carvedilol (25 mg X 2 and 50 mg X 2) showed a useful antihypertensive effect. After 29 days, however, it was still possible to demonstrate an acute decrease in resistance with carvedilol (50 mg) after tablet intake, indicating the vasodilating activity of this compound. When patients with essential hypertension were exposed to an even broad band noise (100 dBA), there was a rise in blood pressure due to an increase in TPR. Alpha 1-adrenoceptor blockade (prazosin 2 mg) prevented the rise in TPR but blood pressure increased in spite of this due to a rise in CO. Moreover, nonselective beta-adrenoceptor blockade and alpha 1-adrenoceptor blockade in combination (labetalol 200 mg) were unable to prevent the rise in blood pressure induced by noise. Finally, precapillary vasodilatation and beta-adrenoceptor blockade (prizidilol 400 mg) given as long-term treatment were also inefficient in preventing the noise-induced (105 dBA) rise in blood pressure. The absolute level of blood pressure obtained, however, was significantly lower than during placebo administration.