• Lancet · Apr 2004

    Increased neuronal nitric oxide synthase-derived NO production in the failing human heart.

    • Thibaud Damy, Philippe Ratajczak, Ajay M Shah, Emmanuel Camors, Isabelle Marty, Gerd Hasenfuss, Françoise Marotte, Jane-Lise Samuel, and Christophe Heymes.
    • INSERM U572 Hôpital Lariboisière, IFR J Marrey Paris-7, 41 Boulevard de la Chapelle, 75475 Paris Cedex 10, Université D Diderot, Paris, France.
    • Lancet. 2004 Apr 24; 363 (9418): 1365-7.

    AbstractExperimental data suggest that nitric oxide (NO) generated from neuronal NO synthase (nNOS) modulates the myocardial inotropic state. To assess the contribution of NO, derived from endothelial and neuronal isoforms, to the pathophysiology of congestive heart failure in human beings, we compared expression, localisation, and specific activity of NOS isoforms in myocardium from patients with dilated cardiomyopathy with those in controls who had died from head trauma or intracranial bleeds. Diseased hearts had a significant increase in nNOS mRNA and protein expression, and activity associated with the translocation of nNOS to the sarcolemma through interactions with caveolin 3. Enhanced nNOS activity counteracted a decrease in eNOS expression and activity. Our results provide evidence of increased nNOS-derived NO in the failing human heart. Such altered regulation may be important in the pathophysiology of cardiac dysfunction in human congestive heart failure.

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