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Nitric Oxide and the Heart: Update on New Paradigms
C. BELGE,
PAUL B. MASSION,
M. PELAT AND
J. L. BALLIGAND
Department of Pharmacology and Therapeutics, Université Catholique de Louvain, Brussels 1200, Belgium
Address for correspondence: Prof. J.L. Balligand, M.D., Ph.D., Unit of Pharmacology and Therapeutics, FATH 5349, Faculty of Medicine, Université Catholique de Louvain (UCL), 53 Avenue Mounier, 1200 Brussels, Belgium. Voice: 32-2-764 5349; fax: 32-2-764 9322. balligand{at}mint.ucl.ac.be
The role of nitric oxide (NO) as a regulator of cardiac contraction was suggested in the early nineties, but a consensual view of its main functions in cardiac physiology has only recently emerged with the help of experiments using genetic deletion or overexpression of the three nitric oxide synthase (NOS) isoforms in cardiomyocytes. Contrary to the effects of exogenous, pharmacologic NO donors, signaling by endogenous NO is restricted to intracellular effectors co-localized with NOS in specific subcellular compartments. This both ensures coordinate signaling by the three NOS isoforms on different aspects of the cardiomyocyte function and helps to reconcile previous apparently contradictory observations based on the use of non-isoform-specific NOS inhibitors. This review will emphasize the role of NOS on excitation-contraction coupling in the normal and diseased heart. Endothelial NOS and neuronal NOS contribute to maintain an adequate balance between adrenergic and vagal input to the myocardium and participate in the early and late phases of the Frank-Starling adaptation of the heart. At the early phases of cardiac diseases, inducible NOS reinforces these effects, which may become maladaptive as disease progresses.
Key Words: excitation-contraction coupling • inhibitors • NO • NOS
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