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Research Article Free access | 10.1172/JCI105667
Department of Medicine and the Argonne Cancer Research Hospital, The University of Chicago, Chicago, Illinois§
‡Present address: The Rockefeller University Hospital, New York, N. Y. 10021.
*Received for publication 15 May 1967 and in revised form 10 July 1967.
Supported in part by U. S. Public Health Service Training Grant TI AM 5445-03.
Presented in part at the Forty-seventh Annual Meeting of the Endocrine Society, New York, N. Y., 17-19 June 1965.
§Operated by the University of Chicago for the United States Atomic Energy Commission.
Address request for reprints to Dr. Fred H. Katz, Department of Medicine, Loyola University Stritch School of Medicine, Hines, Ill. 60141.
Find articles by Katz, F. in: PubMed | Google Scholar
Department of Medicine and the Argonne Cancer Research Hospital, The University of Chicago, Chicago, Illinois§
‡Present address: The Rockefeller University Hospital, New York, N. Y. 10021.
*Received for publication 15 May 1967 and in revised form 10 July 1967.
Supported in part by U. S. Public Health Service Training Grant TI AM 5445-03.
Presented in part at the Forty-seventh Annual Meeting of the Endocrine Society, New York, N. Y., 17-19 June 1965.
§Operated by the University of Chicago for the United States Atomic Energy Commission.
Address request for reprints to Dr. Fred H. Katz, Department of Medicine, Loyola University Stritch School of Medicine, Hines, Ill. 60141.
Find articles by Kappas, A. in: PubMed | Google Scholar
Published November 1, 1967 - More info
The effects of estriol and estradiol on the plasma levels of cortisol- and thyroxine-binding globulin activity, and on the secretion rates of aldosterone and cortisol were studied in man. The metabolite estriol had no consistent or significant influence on plasma levels of the hormone-binding globulin activities; the hormone estradiol increased these binding capacities significantly, as expected. Cortisol secretion rate rose slightly after estriol but was unchanged after estradiol. Both compounds induced substantial increases in the aldosterone secretion rate of most treated subjects. The mechanism of this apparently paradoxical effect of estrogens is not clear; it is suggested that the “salt-retaining” action of estrogens is mediated in part by the rapid enhancement of aldosterone output which follows their administration in man. Balance experiments in four subjects suggest that both estradiol and estriol may induce a transient early natriuresis in man; but other mechanisms for estrogen stimulation of aldosterone secretion may be operative as well.