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The adrenal medullary hormones, I-epinephrine and l-norepinephrine, elicit differing systemic hemodynamic responses when administered in physiologic dosage to normal man (2, 3). Both produce an elevation in the arterial pressure but l-epinephrine does so by increasing cardiac output in association with diminished or unchanging peripheral vascular resistance, whereas I-norepinephrine usually induces a fall in cardiac output and an increase in resistance. Both evoke renal vasoconstriction and a reduction in renal blood flow (4-6) with a decrease in the urinary concentration and excretion of sodium and potassium (7, 8). Since glomerular filtration is not affected (5-9) the reduction in electrolyte output may be ascribed to augmented tubular reabsorption. The urine flow remains essentially unchanged or increases during intravenous infusion of either agent and usually declines abruptly upon termination of the pressor response. These alterations in urine formation may be ascribed to a direct action of the adrenal medullary hormones upon the tubular cellular processes of salt and water transfer or to an indirect effect upon tubular function mediated by release of adrenal cortical hormones or neurogenic activity. The change in urine flow may reflect a secondary change in the production of the antidiuretic hormone (ADH) by the posterior pituitary. The possibility that local renal hemodynamic adjustments also play an important role cannot be excluded. The study reported in this paper was un

A Study of the Mode of Action of the Adrenal Medullary Hormones on Sodium, Potassium and Water Excretion in Man12