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(Hypertension. 2006;47:e20.)
© 2006 American Heart Association, Inc.

Letters to the Editor

Leptin, Endothelin, NADPH Oxidase, and Heart Failure

Division of Vascular Endothelium and Microcirculation, Department of Medicine, Medical Faculty Carl Gustav Carus, University of Technology Dresden, Dresden, Germany

Stefan R. Bornstein

Department of Medicine, Medical Faculty Carl Gustav Carus, University of Technology Dresden, Dresden, Germany

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

To the Editor:

We read with great interest the article by Dong et al¹ in the February 2006 issue of Hypertension. They showed that leptin suppresses cardiac contractile function in ventricular myocytes by an endothelin-1 and NADPH oxidase–dependent pathway.

Interestingly, both endothelin receptor A and B antagonists were able to attenuate the cardiac functional abnormalities in response to leptin. In human myocardium, mainly the endothelin receptor A is functionally important and upregulated by heart failure.² Furthermore, we found that patients with New York Heart Association stage III have, even independent of body mass index, higher leptin levels than New York Heart Association II patients and normal subjects.³ The impaired contractility in response to leptin observed by Dong et al¹ in vitro could also play a role in the decreased ventricular function of obese patients with heart failure.

We found an induction of NADPH oxidase subunit expression and superoxide anion formation by endothelin-1 in human endothelial cells.⁴ Furthermore, transgenic endothelium-restricted overexpression of human endothelin-1 caused increased oxidative stress, augmented activity and expression of vascular NADPH oxidase, vascular remodeling, and endothelial dysfunction.⁵ Therefore, augmented endothelin levels observed in obese patients could increase superoxide anion formation in the vascularized myocardial tissue in vivo by an additional mechanism and could further potentiate the suppressive effect on cardiac contractile function.

Dong et al¹ analyzed the subunit expression of the classical NADPH oxidase complex. Recently, several additional NADPH oxidase complexes have been discovered. Some of these novel NADPH oxidase complexes are involved in development and . . . [Full Text of this Article]

Feng Dong; Xiaochun Zhang; Jun Ren

Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, Wyoming

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