Department of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas†
Address requests for reprints to Dr. Norman M. Kaplan, Dept. of Internal Medicine, The University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, Texas 75235.*
Submitted for publication August 5, 1966; accepted January 4, 1967.
Presented in part at the 38th Annual Meeting of the Central Society for Clinical Research, November 5, 1965, and the endocrinology sectional meeting of the American Society for Clinical Investigation and the American Federation for Clinical Research, May 1, 1966.
Supported by grants from the Dallas Heart Association and the U. S. Public Health Service, National Institute of Arthritis and Metabolic Diseases (AM 06938-04) and General Medical Sciences (NIH 5T01 GM 1421 01).
Published May 1, 1967 - More info
The content of aldosterone, corticosterone, and cortisol has been assayed in normal adrenal tissue obtained at autopsy and in adrenal adenomas from both normotensive and hypertensive patients obtained at autopsy and from patients with primary aldosteronism obtained at surgery. The content of aldosterone and corticosterone in the adenomas of patients with essential hypertension was similar to that of normal adrenal tissue and much less than that of adenomas from patients with primary aldosteronism.
Since these results do not appear to reflect various extraneous factors such as assay technique, degradation of steroids, and patient selection, they suggest that most adrenal adenomas found in patients with essential hypertension are not associated with increased aldosterone production. The presence of such adenomas should not, in itself, be considered evidence for primary aldosteronism.
The excretion or secretion of aldosterone in 43 hypertensive patients was found to be similar to that of 39 normotensive patients. These results suggest that primary aldosteronism is rarely the cause of “essential” hypertension.