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(Hypertension. 2007;49:763.)
© 2007 American Heart Association, Inc.
Editorial Commentaries |
From the William S. Middleton Memorial Veterans Hospital and Departments of Medicine and Pharmacology, School of Medicine and Public Health, University of Wisconsin, Madison.
Correspondence to Theodore L. Goodfriend, Research Service, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terr, Madison, WI 53705. E-mail Theodore.goodfriend@med.va.gov
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
"Be Not Too Fast to Cast the Old Aside"*
Hypertensive patients are said to be resistant to therapy when their pressures exceed goal despite treatment with 3 antihypertensive drugs. The tendency of most clinicians is to treat resistant patients with stronger and stronger agents in higher and higher doses. By contrast, a few reports in the literature suggest surprising usefulness of spironolactone, a relatively weak diuretic, in resistant hypertension.16 In this issue of Hypertension, Chapman et al7 describe the largest reported cohort of resistant hypertensive subjects who responded to spironolactone. The average fall in blood pressure was
22/10 mm Hg on 25 mg per day, quite a noteworthy effect for a low dose of a reputedly feeble old agent, especially when added to 3 newer drugs with better reputations! Whats more, the resistant patients who responded to spironolactone included older subjects with predominantly systolic hypertension, many of whom were diabetic, a notoriously recalcitrant group.
Spironolactone antagonizes aldosterone and other salt-retaining steroids by competing for the mineralocorticoid receptor. This action is the simplest but not the only plausible explanation for the efficacy of spironolactone, and it implies that aldosterone plays an unusually prominent role in supporting the pressure of resistant patients. If aldosterone caused resistance, one might assume that those patients were producing a lot of it, but it is unlikely that a dose of 25 mg of spironolactone could have had dramatic effects as an aldosterone antagonist if the endogenous steroid levels were very high. Clinical experiments teach that
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