Adequate oral or intravenous doses of a betaadrenergic receptor-blocking drug, nethalide,' produce no significant changes in the resting oxygen consumption, heart rate, cardiac output, and systemic mean arterial or mean right atrial pressures of patients with spontaneous hyperthyroidism (1). These findings do not support the concept that the hemodynamic changes in hyperthyroidism are mediated through adrenergic stimulation of betaadrenergic receptors. The work of Brewster, Isaacs, Osgood, and King, however, supported the hypothesis that the sympathetic nervous system may be responsible for the metabolic and hemodynamic changes associated with the hypermetabolic state, since the alterations induced by thyroid feeding to dogs could be abolished by epidural blockade (2). The possibility exists that spontaneous hyperthyroidism and drug-induced hypermetabolism may have similar hemodynamic findings but different mechanisms. This study was designed to test the effects of beta-adrenergic blockade in normal subjects before, during, and after the induction of hypermetabolism with triio-