Role of Nitric Oxide in the Pathophysiology of Heart Failure

被引：0
作者：
Hunter C. Champion
Michel W. Skaf
Joshua M. Hare
机构：
[1] Johns Hopkins Hospital,Division of Cardiology, Department of Medicine
来源：
Heart Failure Reviews | 2003年 / 8卷
关键词：
nitric oxide; heart failure; spatial compartmentalization; myocyte;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Nitric oxide (NO) plays critical roles in the regulation of integrated cardiac and vascular function and homeostasis. An understanding of the physiologic role and relative contribution of the three NO synthase isoforms (neuronal—NOS1, inducible—NOS2, and endothelial—NOS3) is imperative to comprehend derangements of the NO signaling pathway in the failing cardiovascular system. Several theories of NO and its regulation have developed as explanations for the divergent observations from studies in health and disease states. Here we review the physiologic and pathophysiologic influence of NO on cardiac function, in a framework that considers several theories of altered NO signaling in heart failure. We discuss the notion of spatial compartmentalization of NO signaling within the myocyte in an effort to reconcile many controversies about derangements in the influences of NO in the heart and vasculature.
引用
收藏
页码：35 / 46
页数：11
相关论文
共 650 条
  • [1] Stamler JS(2001)Nitrosylation. The prototypic redox-based signaling mechanism Cell 106 675-683
  • [2] Lamas S(1999)Modulator, not mediator of cardiac performance Nat Med 5 273-274
  • [3] Fang FC(2002)Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms Nature 416 337-339
  • [4] Hare JM(1997)Nitric oxide synthases: Which, where, how and why? J Clin Invest 100 2146-2152
  • [5] Stamler J. N(1996)Mitochondrial nitric oxide synthase: A ubiquitous regulator of oxidative phosphorylation? Biochem Biophys Res Comm 218 40-44
  • [6] Barouch LA(1999)BeckerLC.NOsynthase in cardiac sarcoplasmic reticulum Proc Natl Acad Sci USA 96 657-662
  • [7] Harrison RW(2001)Augmented age-associated innate immune responses contribute to negative inotropic and lusitropic effects of lipopolysaccharide and interferon gamma JMol Cell Cardiol 33 1849-1859
  • [8] Skaf MW(2002)Disruption of inducible nitric oxide synthase improves betaadrenergic inotropic responsiveness but not the survival of mice with cytokine-induced cardiomyopathy Circ Res 90 959-965
  • [9] Rosas GO(1998)Increased sensitivity to nitric oxide synthase inhibition in patients with heart failure: Potentiation of ?-adrenergic inotropic responsiveness Circulation 97 161-166
  • [10] Cappola TP(1998)Reduced nitric oxide production and altered myocardial metabolism during the decompensation of pacing-induced heart failure in the conscious dog Circ Res 83 969-979
12345678910