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Am J Physiol Regul Integr Comp Physiol 292: R731-R735, 2007. First published July 20, 2006; doi:10.1152/ajpregu.00353.2006
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Sex Differences in Renal and Cardiovascular Function: Physiology and Pathophysiology

Impact of androgen-induced oxidative stress on hypertension in male SHR

Radu Iliescu,* Valeria E. Cucchiarelli,* Licy L. Yanes, Joshua W. Iles, and Jane F. Reckelhoff

Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi

Submitted 25 May 2006 ; accepted in final form 17 July 2006

Men have higher blood pressure than women, and androgens and oxidative stress have been implicated as playing roles in this sexual dimorphism. The spontaneously hypertensive rat (SHR) is an animal model of both androgen- and oxidative stress-mediated hypertension. Therefore, the present studies were performed to test the hypothesis that androgens cause hypertension in SHR in part by stimulating superoxide production via NADPH oxidase. Castration of male SHR reduced blood pressure by 15% and attenuated both basal and NADPH-stimulated superoxide production in kidney cortical homogenates. Expression of p47phox and gp91phox but not p22phox subunits of NADPH oxidase were significantly lower in kidney cortex from castrated males compared with intact males. Moreover, inhibition of NADPH oxidase with apocynin caused ~15 mmHg reduction in blood pressure and reduced basal and NADPH-stimulated superoxide production in intact male SHR, but had no effect on blood pressure or superoxide production in castrated males. These data support the hypothesis that androgens cause oxidative stress and thereby increase blood pressure in male SHR via an NADPH oxidase-dependent mechanism.

hypertension; oxidative stress; androgens; superoxide anion; spontaneously hypertensive rat


Address for reprint requests and other correspondence: J. F. Reckelhoff, Dept. of Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 N. State St., Jackson, MS 39216-4505 (e-mail: jreckelhoff{at}physiology.umsmed.edu)




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