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In the heart, nitric oxide synthases (NOS) modulate cardiac contraction in an isoform-specific manner, which is critically dependent on their cellular and subcellular localization. Defective NO production by NOS3 (endothelial NOS [eNOS]) in the failing heart may precipitate cardiac failure, which could be reversed by overexpression of NOS3 in the myocardium.

circulation

Cardiomyocyte-Restricted Overexpression of Endothelial Nitric Oxide Synthase ( <i>NOS3</i> ) Attenuates β-Adrenergic Stimulation and Reinforces Vagal Inhibition of Cardiac Contraction

Cardiomyocyte-Restricted Overexpression of Endothelial Nitric Oxide Synthase ( NOS3 ) Attenuates β-Adrenergic Stimulation and Reinforces Vagal Inhibition of Cardiac Contraction