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J. C. BECK, M.D.; I. DYRENFURTH, M.D.; C. GIROUD, M.D.; E. H. VENNING, Ph.D.

AMA Arch Intern Med. 1955;96(4):463-469.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

The regulatory mechanisms governing aldosterone secretion in man are as yet obscure. Axelrad and Leutscher ¹ have shown that a fivefold increase in urinary aldosterone occurs in man when the dietary sodium is restricted. Laragh and Stoerk² have suggested that serum potassium is a powerful direct or indirect stimulus to aldosterone secretion and that increases in urinary aldosterone on dietary sodium restriction are mediated by an alteration in serum potassium or Na/K ratio. Although corticotropin does not appear to affect either the excretion * or the blood levels of aldosterone in normal persons,⁴ Gordon and co-workers ⁵ have found an increase in the output of this sodiumretaining hormone in a patient with rheumatoid arthritis following the intravenous administration of corticotropin. Leutscher and Axelrad ⁶ have observed essentially normal levels of urinary aldosterone in patients with panhypopituitarism. It has been sug- gested by Peters ⁷ that the mineralocorticoid output of . . . [Full Text PDF of this Article]

Author Affiliations
Montreal, Canada

From the McGill University Clinic, Royal Victoria Hospital; Markle Scholar (Dr. Beck).

Footnotes
Submitted for publication July 7, 1955.

Read at the Sixty-Eighth Annual Meeting of the Association of American Physicians, Atlantic City, N. J., May 3, 1955.

Supported by Grants from the National Research Council of Canada; Department of the Army Medical Research and Development Board, Washington, D. C., and Eli Lilly & Company, Indianapolis.

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