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Urinary Free 19–Nor–Deoxycorticosterone and Deoxycorticosterone in Human Hypertension^*

Departments of Internal Medicine, University of South Florida College of Medicine, and the Department of Medicine, James A. Haley Veterans Administration Hospital Tampa, Florida
University of Texas Medical Branch Galveston, Texas 77550

Address all correspondence and requests for reprints to: Celso E. Gomez-Sanchez, M.D., Tampa Veterans Administration Hospital, 13000 North 30th Street VAH 111–M, Tampa, Florida 33612.

The urinary excretion of deoxycorticosterone (DOC) and 19–nor–deoxycorticosterone (19–nor–DOC) was measured using a technique which consisted of the purification of both steroids by high pressure liquid chromatography followed by RIA using specific antibodies. The urinary excretion of DOC was 29.4 ± 25 ng/24 h (mean ± SD) in 35 normal subjects, 26 ± 21 ng/24 h in 46 patients with low renin hypertension (LRHT), and 32 ± 23 ng/24 h in 16 patients with normal renin hypertension (NRHT). The urinary excretion of 19–nor–DOC was 287 ± 178 ng/24 h in normal subjects, 224 ± 167 ng/24 h in LRHT patients, and 235 ± 170 ng/24 h in NRHT patients. There were no hypertensive patients with increased excretion of 19–nor–DOC. The excretion of 19–nor–DOC increased after 3 days of sodium depletion in normal and hypertensive subjects, but the increment was significantly higher in normotensive subjects. There was no correlation between the excretion of 19–nor–DOC and that of DOC or urinary aldosterone. This study suggests that DOC or 19–nor–DOC does not play a role in the pathogenesis of either LRHT or NRHT and disagrees with previous reports suggesting such a role.

^* This work was supported by research funds from the V.A., the NIH (HL–27255 and HL–26856) and its General Clinical Research Centers Program of the Division of Research Resources (RR–633 and RR–73), and the American Heart Association and its Texas Affiliate.

Received March 28, 1984.

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