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Neuronal nitric oxide synthase (nNOS) is considered a regulator of Ca v 1.2 L-type Ca 2+ channels and downstream Ca 2+ cycling in the heart. The commonest view is that nitric oxide (NO), generated by nNOS activity in cardiomyocytes, reduces the currents through Ca v 1.2 channels. This gives rise to a diminished Ca 2+ release from the sarcoplasmic reticulum, and finally reduced contractility. Here, we report that nNOS inhibitor substances significantly increase intracellular Ca 2+ transients in ventricular cardiomyocytes derived from adult mouse and rat hearts. This is consistent with an inhibitory effect of nNOS/NO activity on Ca 2+ cycling and contractility. Whole cell currents through L-type Ca 2+ channels in rodent myocytes, on the other hand, were not substantially affected by the application of various NOS inhibitors, or application of a NO donor substance. Moreover, the presence of NO donors had no effect on the single-channel open probability of purified human Ca v 1.2 channel protein reconstituted in artificial liposomes. These results indicate that nNOS/NO activity does not directly modify Ca v 1.2 channel function. We conclude that-against the currently prevailing view-basal Ca v 1.2 channel activity in ventricular cardiomyocytes is not substantially regulated by nNOS activity and NO. Hence, nNOS/NO inhibition of Ca 2+ cycling and contractility occurs independently of direct regulation of Ca v 1.2 channels by NO.

pflügers archiv für die gesamte physiologie des menschen und der tiere/pflügers archiv

Neuronal nitric oxide synthase regulation of calcium cycling in ventricular cardiomyocytes is independent of Cav1.2 channel modulation under basal conditions