S-Nitrosylation-Mediated Reduction of Ca1.2 Surface Expression and Open Probability Underlies Attenuated Vasoconstriction Induced by Nitric Oxide.

Background: L-type Ca1.2 calcium channel, the primary gateway for Ca influx in smooth muscles, is widely regulated by multiple posttranslational modifications, such as protein kinase-mediated phosphorylation and nitric oxide-induced S-nitrosylation. However, the effect of S-nitrosylation on Ca1.