Dependence of cardiac function upon sympathetic nervous outflow to the heart has been studied until recently by means of surgical interruption of nerve pathways. The introduction of beta adrenergic blocking agents such as propranolol has made it possible to achieve specific "pharmacologic sympathectomy." Initial studies reveal that drug blockade of beta adrenergic receptors results in reduction of cardiac response to exercise. This inability to increase cardiac output appropriately in response to increased metabolic demand is a prominent manifestation of impaired cardiac function. Another major manifestation of decreased hemodynamic performance is the diminished ability to excrete sodium. Does beta adrenergic blockade also result in impairment of sodium excretion?
Epstein and Braunwald1 have recently described the effects of the oral administration of propranolol on urinary sodium excretion in both normal subjects and patients with heart disease. Beta blockade altered the pattern of sodium excretion in all individuals so that a greater percentage