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February 1974

Low-Renin Hypertension: Restoration of Normotension and Renin Responsiveness

Author Affiliations


From the Steroid Research Laboratory, Endocrine Unit (Dr. Spark), Harvard Medical School, Beth Israel Hospital, Boston.

Arch Intern Med. 1974;133(2):205-211. doi:10.1001/archinte.1974.00320140043004

Ten patients with low-renin hypertension were treated with high doses of a diuretic and a mineralocorticoid antagonist in a double-blind crossover study. Hydrochlorothiazide-induced volume depletion had a beneficial hypotensive response. However, despite comparable diuretic response, the hypotensive response observed with spironolactone was significantly greater. Renin responsiveness was seen to increase—but to submaximal levels—with thiazide therapy; while spironolactone therapy restored normal renin responsiveness. The differential response to thiazide and spironolactone is similar to the response observed when these agents are used in primary aldosteronism, a hypertensive disease where mineralocorticoid excess is clearly identified as the cause of both the hypertension and low plasma renin activity. The fact that mineralocorticoid blockade induced by spironolactone corrects the hypertension and restores normal renin responsiveness suggests that mineralocorticoid excess may be responsible for the hypertension and low plasma renin activity.

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