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Nitric Oxide Increases Cardiac IK1 by Nitrosylation of Cysteine 76 of Kir2.1 Channels
Circulation Research, 07/21/09

Gómez R et al. – The results demonstrated that, under physiological conditions, NO regulates human cardiac IK1 through a redox–related process.

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Ricardo Caballero, 07/22/09

We demonstrate that NO, at physiological concentrations, increases the human cardiac inward rectifier current IK1 generated by Kir2.1 channels by augmenting the open probability of the channel as a result of the S-nitrosylation of the Cys76 residue. The findings provide a deeper insight into the modulation of cardiac IK1 and describe, for the first time, an important mechanism by which NO participates in the regulation of cardiac RMP and in shaping APs.

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