Nitric Oxide and Cardiac Function

  • P.B. Massion
    From the Department of Medicine, Unit of Pharmacology and Therapeutics (FATH 5349), University of Louvain Medical School, Brussels, Belgium.
  • O. Feron
    From the Department of Medicine, Unit of Pharmacology and Therapeutics (FATH 5349), University of Louvain Medical School, Brussels, Belgium.
  • C. Dessy
    From the Department of Medicine, Unit of Pharmacology and Therapeutics (FATH 5349), University of Louvain Medical School, Brussels, Belgium.
  • J.-L. Balligand
    From the Department of Medicine, Unit of Pharmacology and Therapeutics (FATH 5349), University of Louvain Medical School, Brussels, Belgium.

書誌事項

タイトル別名
  • Ten Years After, and Continuing

説明

<jats:p>Nitric oxide (NO) is produced from virtually all cell types composing the myocardium and regulates cardiac function through both vascular-dependent and -independent effects. The former include regulation of coronary vessel tone, thrombogenicity, and proliferative and inflammatory properties as well as cellular cross-talk supporting angiogenesis. The latter comprise the direct effects of NO on several aspects of cardiomyocyte contractility, from the fine regulation of excitation-contraction coupling to modulation of (presynaptic and postsynaptic) autonomic signaling and mitochondrial respiration. This multifaceted involvement of NO in cardiac physiology is supported by a tight molecular regulation of the three NO synthases, from cellular spatial confinement to posttranslational allosteric modulation by specific interacting proteins, acting in concert to restrict the influence of NO to a particular intracellular target in a stimulus-specific manner. Loss of this specificity, such as produced on excessive NO delivery from inflammatory cells (or cytokine-stimulated cardiomyocytes themselves), may result in profound cellular disturbances leading to heart failure. Future therapeutic manipulations of cardiac NO synthesis will necessarily draw on additional characterization of the cellular and molecular determinants for the net effect of this versatile radical on the cardiomyocyte biology.</jats:p>

収録刊行物

  • Circulation Research

    Circulation Research 93 (5), 388-398, 2003-09-05

    Ovid Technologies (Wolters Kluwer Health)

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