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Hypertension. 1998;32:376-377

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(Hypertension. 1998;32:376-377.)
© 1998 American Heart Association, Inc.


Letters to the Editor

Leptin and the Renin-Angiotensin-Aldosterone System

Stefan R. Bornstein; ; David J. Torpy

National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Md

To the Editor:

Shek et al1 recently reported in a very detailed study that chronic leptin infusion in rats increased mean arterial blood pressure. However, the mechanism of leptin-induced hypertension is unclear and may involve both central and peripheral actions. While the sympathoexcitatory action of leptin is well established and may be a major factor mediating its hypertensive effect,1 2 the role of leptin in another major regulator of blood pressure, the renin-angiotensin-aldosterone system, has yet to be defined. Shek et al provide the first data on renin and aldosterone levels after leptin treatment in vivo.1 Whereas renin levels were unchanged, aldosterone tended to decrease at higher doses. In accordance with these findings, previous studies have shown that infusion of leptin caused natriuresis and diuresis.3 The authors suggest that reduced plasma aldosterone levels may be due to reduced potassium intake associated with leptin-induced anorexia. We suggest that a more likely explanation is a direct effect of leptin on the adrenal cortex. We have previously demonstrated in primary adrenal cell cultures that leptin can directly inhibit adrenocortical steroid production and the mRNA expression of cytochrome P450 enzymes.4 Therefore, leptin can chronically depress steroid production at the level of the adrenal, which is in line with the in vivo data reported in this study. In addition, our preliminary data demonstrate a slight increase in plasma renin activity in rats chronically treated with leptin (0.12 mg/kg per day IP over 7 days). In treated animals, we observed a trend toward increased plasma renin activity . . . [Full Text of this Article]

Eugene W. Shek; Michael W. Brands; ; John E. Hall

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Miss




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