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(Hypertension. 2007;50:840.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Mineralocorticoid Receptor Activation and Oxidative Stress

John W. Funder

From Prince Henry’s Institute of Medical Research, Clayton, Victoria, Australia.

Correspondence to Professor John W. Funder, Prince Henry’s Institute of Medical Research, Monash Medical Centre, 246 Clayton Road, PO Box 5152, Clayton, Victoria, Australia 3168. E-mail John.Funder@princehenrys.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The spontaneously hypertensive rat (SHR) has been extensively used in studies of hypertension for decades. More recently, a leptin receptor–deficient SHR (SHR/NDmer-cp; SHR/cp) has been developed as a model for the human metabolic syndrome, characterized by elevated blood pressure, visceral obesity, glucose intolerance, and dyslipidemia. In this issue of Hypertension Nagase et al¹ have used the SHR/cp to explore the role of oxidative stress and mineralocorticoid receptor (MR) activation on the renal damage that follows a forced high salt intake. The authors have examined an impressive array of markers of renal structural and functional damage, and show that the antioxidant tempol (partially) and the selective MR antagonist eplerenone (completely) block the renal damage caused by 8% NaCl as drinking solution.

In sodium deficiency states aldosterone levels are very high, and MR is very much activated, as evidenced by high levels of sodium retention; in such circumstances, however, no vascular or tubular damage is seen. In contrast, when mineralocorticoid levels are inappropriately high for sodium status—in Conn’s syndrome or experimentally (DOC/salt, aldo/salt rat models)—progressive vascular damage occurs in tissues, some of which are classic aldosterone targets (eg, kidney) and others are not (eg, heart). How MR activation in salt deficiency is homeostatic, whereas in sodium loading it is unambiguously deleterious, is a key question yet to be answered. The data in the Nagase et al article show first that the deleterious effects of salt loading are absolutely dependent on MR activation. Secondly, they show that such activation reflects reactive oxygen species . . . [Full Text of this Article]

Related Article:

Salt-Induced Nephropathy in Obese Spontaneously Hypertensive Rats Via Paradoxical Activation of the Mineralocorticoid Receptor: Role of Oxidative Stress

Miki Nagase, Hiromitsu Matsui, Shigeru Shibata, Takanari Gotoda, and Toshiro Fujita
Hypertension 2007 50: 877-883. [Abstract] [Full Text] [PDF]

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