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Endocrine-Metabolic Unit and Department of Medicine, Peter Bent Brigham Hospital and Harvard Medical School Boston, Massachusetts
2 Address reprint requests to: Dr. Gordon H. Williams, Peter Bent Brigham Hospital, 721 Huntington Avenue, Boston, Massachusetts 02115.
The control of aldosterone secretion was investigated in 23 hyperthyroid patients. Compared to normal subjects, chronically sodium restricted hyperthyroid patients had blunted aldosterone secretion (645 ± 73 µg/day); low plasma aldosterone (47 ±4 ng/100 ml); increased estimated aldosterone metabolic clearance rate (2230 ± 284 L/day); and increased plasma renin activity (32.7 ± 3.5 ng/ml/3 hr). Renin and aldosterone responses during ACTH and saline loading were normal, and oral potassium loading normalized aldosterone secretion and lowered renin activity. Propranolol significantly lowered renin activity but not aldosterone secretion. The elevated plasma renin activity was probably secondary to increased sympathetic stimulation and potassium depletion. It is likely that potassium depletion also contributed to the blunted aldosterone secretion during sodium deprivation.
1 Present Address: University Hospital, London, Ontario, Canada.
Received May 17, 1972.
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