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Research Article Free access | 10.1172/JCI107414
Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
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Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
Find articles by Weinberger, M. in: JCI | PubMed | Google Scholar
Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
Find articles by Gomez-Sanchez, C. in: JCI | PubMed | Google Scholar
Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
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Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
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Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
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Departments of Internal Medicine, The University of Texas Southwestern Medical School, Dallas, Texas 75235
Indiana University Medical School, Indianapolis, Indiana
University of Arizona, College of Medicine, Tucson, Arizona.
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Published September 1, 1973 - More info
Plasma aldosterone, cortisol, and renin activity were measured in nine recumbent patients with hyperaldosteronism, including seven with adenomas, one with idiopathic hyperplasia, and one with glucocorticoid suppressible hyperplasia. All had peak values of plasma aldosterone concentration from 3 a.m. to noon and lowest values at 6 p.m. or midnight. This rhythm was similar to the circadian pattern of plasma cortisol in the same patients. When these data were normalized to eliminate the wide variation in ranges of plasma aldosterone and cortisol between individuals, there was an excellent correlation (r = + 0.87, P < 0.005) between the two hormones. In contrast, plasma aldosterone concentrations did not correlate with plasma renin activity before or after normalization of data.
Short term suppression of ACTH by administration of dexamethasone eliminated the circadian variation of plasma aldosterone in both patients with hyperplasia and in four of five patients with adenomas, while it markedly altered the rhythm in the fifth. Similar doses of dexamethasone were administered to four normal subjects and did not flatten the circadian rhythm of plasma aldosterone.
These data suggest that patients with primary aldosteronism have a circadian rhythm of plasma aldosterone mediated by changes in ACTH.