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Whereas nitric oxide (NO) has been implicated in the pathophysiology of heart failure (HF), the significance and functional role of different NO synthase (NOS) isoforms in this pathology are controversial. Our aim was to study in the myocardium of rats with volume-overload-induced HF the expression, activity, and localization of endothelial (eNOS) and inducible (iNOS) isoforms and the involvement of iNOS in depressed cardiac contractile properties, intracellular Ca(2+) ([Ca(2+)](i)) transients, and beta-adrenergic hyporesponsiveness.

circulation

Role of Myocardial Inducible Nitric Oxide Synthase in Contractile Dysfunction and β-Adrenergic Hyporesponsiveness in Rats With Experimental Volume-Overload Heart Failure