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Emerging evidence shows that neuronal nitric oxide synthase (nNOS) plays several diverging roles in modulating cardiac function. This review examines the nitric oxide (NO) pathway and the regulatory mechanisms to which nNOS signalling is sensitive. These mechanisms are diverse and include regulation of gene expression, posttranscriptional regulation, protein trafficking, allosteric modulation of nNOS and redox modification to alter NO bioavailability once synthesised. Functionally, alteration in nNOS-NO signalling in the heart may correlate with different cardiac regulatory states. The idea of this being associated with exercise-trained states and myocardial disease is discussed.

Original publication




Journal article


Pharmacol Ther

Publication Date





57 - 74


Allosteric Regulation, Animals, Gene Expression Regulation, Enzymologic, Heart, Humans, Myocardium, Nerve Tissue Proteins, Nitric Oxide, Nitric Oxide Synthase, Nitric Oxide Synthase Type I, Oxidation-Reduction, Protein Transport, Signal Transduction