Renal Tubular Effects of Hydrocortisone and Aldosterone in Normal Hydropenic Man: Comment on Sites of Action *

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Abstract
Changes in urine solute concentration, urine urea concentration, electrolyte excretion, and renal hemodynamics produced in normal hydropenic subjects by the intravenous administration of hydrocortisone and aldosterone were compared to those produced by a placebo injection administered under the same experimental conditions. Hydrocortisone produced a significant increase in urine osmolality without any alteration in urine flow rate, solute clearance, and urine urea concentration. Aldosterone also increased urine solute concentration but with a significant decrease in urine flow rate and solute clearance. In contrast to hydrocortisone, the increment in urine solute concentration produced by aldosterone was entirely accounted for by the increase in urine urea concentration. Neither hydrocortisone nor aldosterone influenced renal hemodynamics. Hydrocortisone increased K+ excretion and decreased Na+ excretion to a lesser extent. Aldosterone produced a significant reduction in Na+ and Cl excretion with only a minor decrease in K+ excretion. Hydrocortisone increased TcH2O formation in both normal and adrenal-in-sufficient subjects. This parameter was not affected by aldosterone. These data indicate that hydrocortisone enhances Na+ supply and transport at the ascending limb. In contrast, aldosterone appears to enhance directly Na+ and Cl reabsorption in the distal convoluted tubule. Both agents also directly augment the Na+/K+ exchange mechanism in the late distal tubule and collecting duct.