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Am J Physiol Heart Circ Physiol 282: H2159-H2166, 2002. First published February 14, 2002; doi:10.1152/ajpheart.00872.2001
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Vol. 282, Issue 6, H2159-H2166, June 2002

Involvement of inducible nitric oxide synthase in cardiac dysfunction with tumor necrosis factor-alpha

Hajime Funakoshi1, Toru Kubota1, Yoji Machida1, Natsumi Kawamura1, Arthur M. Feldman2, Hiroyuki Tsutsui1, Hiroaki Shimokawa1, and Akira Takeshita1

1 Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan 812-8582; and 2 Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213

Transgenic (TG) mice with cardiac-specific overexpression of tumor necrosis factor (TNF)-alpha develop dilated cardiomyopathy with myocardial inflammation. The purpose of this study was to investigate the role of nitric oxide (NO) in this mouse model of cardiomyopathy. Female TG and wild-type mice at the age of 10 wk were studied. The expression and activity of inducible NO synthase (iNOS) were significantly increased in the TG myocardium, whereas those of endothelial NOS were not altered. The majority of the iNOS protein was isolated in the interstitial cells. The selective iNOS inhibitor (1S,5S,6R,7R)- 7-chloro-3-imino-5-methyl-2-azabicyclo[4.1.0]heptane hydrochloride (ONO-1714) was used to examine the effects of iNOS induction on myocardial contractility. Echocardiography and left ventricular pressure measurements were performed. Both fractional shortening and the maximum rate of rise of left ventricular pressure were significantly suppressed in TG mice. Although ONO-1714 did not change hemodynamic parameters or contractility at baseline, it significantly improved beta -adrenergic inotropic responsiveness in TG mice. These results indicate that induction of iNOS may play an important role in the pathogenesis of cardiac dysfunction in this mouse model of cytokine-induced cardiomyopathy.

cytokine; heart failure; transgenic mice


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