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Suppression of Plasma Renin Activity in Primary AldosteronismDistinguishing Primary From Secondary Aldosteronism in Hypertensive Disease
Jerome W. Conn, MD;
Edwin L. Cohen, MD;
David R. Rovner, MD
JAMA. 1985;253(4):558-566.
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THE OCCURRENCE in a hypertensive patient of increased production of aldosterone, and of the hypokalemia which often accompanies it, is due either to the presence of an aldosterone-secreting adrenocortical tumor (primary aldosteronism), or the presence of a functional renal hemodynamic change which stimulates the renal juxtaglomerular cells to secrete into the blood abnormally large amounts of renin. In the latter case, an increased quantity of angiotensin II is thus generated. Angiotensin II has been established to be a potent stimulus for the secretion of aldosterone by the adrenal cortices of man.1,2 Although increased secretion of aldosterone can be induced in man by other mechanisms, it is now clear that, when hypersecretion of aldosterone occurs in human renal hypertension (secondary aldosteronism), it is the result of increased activity of the renin-angiotensin system. This seems to be true whether the decreased "stretch"3 at the renal baroreceptor site (the juxtaglomerular cells)
. . . [Full Text PDF of this Article]
Author Affiliations
Ann Arbor, Mich
From the Division of Endocrinology and Metabolism and the Metabolism research unit of the Department of Internal Medicine, University of Michigan.
Footnotes
Read in part before the General Scientific Meeting on Hyperfunction of the Endocrine Glands and Functioning Endocrine Tumors during the 113th Annual Meeting of the American Medical Association, San Francisco, June 22, 1964.
Reprint requests to C-7129 University Hospital, University of Michigan Medical Center, Ann Arbor (Dr. Conn).
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