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(Circulation. 2005;111:830-831.)
© 2005 American Heart Association, Inc.

Editorial

Calcium, Magnesium, and Oxidative Stress in Hyperaldosteronism

Ernesto L. Schiffrin, MD, PhD, FRCPC; Rhian M. Touyz, MD, PhD

From the Canadian Institutes of Health Research Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Montreal, Québec, Canada.

Correspondence to Ernesto L. Schiffrin, MD, PhD, FRCPC, Clinical Research Institute of Montreal, 110 Pine Ave W, Montreal, QC H2W 1R7, Canada. E-mail ernesto.schiffrin@ircm.qc.ca

Key Words: Editorials • hyperaldosteronism • calcium • magnesium • reactive oxygen species

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

Hyperaldosteronism has been demonstrated to be associated with magnesium loss in the urine and hypomagnesemia¹ as part of the syndrome of metabolic alkalosis and hypokalemia that characterizes this condition. In this issue of Circulation, Chhokar et al² demonstrate the consequences of metabolic changes in rats subjected to aldosterone infusion in the presence of excess salt that result in hypocalcemia and hypomagnesemia, hyperparathyroidism, bone resorption, and calcium overload of tissues including the heart. This is associated with the enhanced production of reactive oxygen species (ROS) and an inflammatory phenotype, which then contribute to the decline in cardiac function and the progression to heart failure.

See p 871

Our knowledge of the (patho)physiological role of aldosterone and that of magnesium has increased dramatically during the past few years. The finding that aldosterone acts on target tissues other than the classic epithelial cells (kidney, colon) has had a profound influence on our understanding of the significance of aldosterone in cardiovascular disease. Aldosterone is now known to act on the heart and blood vessels, not only on muscle (smooth muscle and cardiomyocytes), but also on endothelial cells, where it induces nuclear swelling,³ which has been implicated in the mechanisms of vascular damage. Part of the effects of aldosterone may be mediated by the upregulation of endothelin-1 gene expression in the vasculature and the heart,⁴ as well as cross-talk with endothelin ET_A receptors at the level of caveolae/lipid rafts.⁵ These effects occur through different mechanisms that may involve NADPH oxidase,⁶ xanthine oxidase,⁷ or mitochondrial . . . [Full Text of this Article]

Related Article:

Hyperparathyroidism and the Calcium Paradox of Aldosteronism

Vikram S. Chhokar, Yao Sun, Syamal K. Bhattacharya, Robert A. Ahokas, Linda K. Myers, Zhiqing Xing, Richard A. Smith, Ivan C. Gerling, and Karl T. Weber
Circulation 2005 111: 871-878. [Abstract] [Full Text]

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