Effects of beta-adrenergic receptor blockade in normal subjects before, during, and after triiodothyronine-induced hypermetabolism.

Abstract

The effect of beta adrenergic receptor blockade (propranolol 0.15 mgAg intravenously) was studied in 8 normal subjects before, during and after a period of triiodothyronine-induced hypermetabolism. Propranolol inhibited the chronotropic and inotropic effects of isoproterenol but did not significantly change the average O2 consumption, heart rate, systemic mean arterial pressure, cardiac output or total systemic resistance in either the hypermetabolic or the 2 control periods. Propranolol did not alter the fall in mean arterial pressure but significantly attenuated the increase in heart rate during inhalation of amyl nitrite in the hypermetabolic and final control periods. The hemodynamic responses to mild exercise were simlar before and after propranolol in each period. Triiodothyronine did not augment the hemodynamic responses to isoproterenol. These studies indicate that the hemodynamic changes in drug-induced hypermetabolism, like those of spontaneous hyper-thyroidism, are not mediated through stimulation of beta adrenergic receptors.