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

Abstract

This study has confirmed previous observations of decreased renal blood flow, unchanged glomerular filtration rate, diminished Na and K excretion and a tendency to loss of water in the urine during the pressor action of intravenous l-norepineph-rine and l-epinephrine in 22 normal human subjects. The change; in urinary electrolyte excretion is apparently not mediated through adrenal cortical activation since 3 patients with adrenal cortical insufficiency responded normally to 1-norepinephrine. Diminished formation of antidiuretic hormone may account for the sustained or augmented output of a dilute urine during infusion of the medullary amines. In a patient with diabetes, 1-norepinephrine depressed both electrolyte and water excretion although Pitressin reduced urine flow without altering electrolyte in 3 normal subjects receiving l-norepinephEine infusion. l-Norepinephrine given during antidiuresis produced by Pitressin effected a decreased electrolyte excretion without changing urine flow in 4 normal subjects indicating the independence of changes in renal tubular electrolyte and water reabsorp-tion. High spinal anesthesia (T 8 or higher) did not interfere with the l-norepinephrine response in 4 normal subjects and l-epineph-rine in doses too small to change arterial blood pressure evoked the typical renal functional alterations in 2 normal subjects. Na and K excretion were lowered by angiotonin (3 subjects) and S-methyl isothiourea (2 subjects) but glomerular filtration rate and urine flow were also decreased during the reduction in renal blood flow. Ephedrine in 4 subjects did not reduce renal blood flow or glomerular filtration but K excretion decreased and Na output increased. Renal tubular Na reabsorption increased in association with a fall in renal blood flow while K retention was correlated only with intrarenal vasoconstriction, suggesting an indirect action of the adrenal medullary hormones on renal tubular cells mediated through local hemodynamic adjustments.