Circulating catecholamines in control of renal electrolyte and water excretion

Graded physiological doses of norepinephrine or epinephrine were infused either intravenously or directly into the renal artery of conscious dogs previously prepared with chronic indwelling catheters. Infusion rates ranged from 5 to 125 ng . kg-1 . min-1, and aortic plasma catecholamine concentrations were measured during intravenous infusion to determine the actual levels achieved. Even when the renal arterial plasma norepinephrine concentration was raised to 5,000 pg/ml by either intravenous or intrarenal infusion, only a modest sodium and potassium retention was observed. Only intravenous norepinephrine increased urinary flow rate. Increments of epinephrine concentration from 120 to 2,000 pg/ml decreased sodium and potassium excretion only when delivered intravenously. The concentrations of norepinephrine or epinephrine required to alter urinary sodium and potassium excretion and flow rate were in the upper physiological range or higher and the responses were small except for intravenous epinephrine, which decreased sodium excretion at very low physiological concentrations (120-400 pg/ml). We conclude that circulating epinephrine may play an important physiological role in renal sodium conservation. This effect of epinephrine is not due to a direct intrarenal mechanism.