Carvedilol inhibits cADPR- and IP₃-induced Ca²⁺ release.

ABSTRACT: Spontaneous Ca²⁺ waves, also termed store-overload-induced Ca²⁺ release (SOICR), in cardiac cells can trigger ventricular arrhythmias especially in failing hearts. SOICR occurs when RyRs are activated by an increase in sarcoplasmic reticulum (SR) luminal Ca²⁺. Carvedilol is one of the most effective drugs for preventing arrhythmias in patients with heart failure. Furthermore, carvedilol analogues with minimal β-blocking activity also block SOICR showing that SOICR-inhibiting activity is distinct from that for β-block. We show here that carvedilol is a potent inhibitor of cADPR-induced Ca²⁺ release in sea urchin egg homogenate. In addition, the carvedilol analog VK-II-86 with minimal β-blocking activity also suppresses cADPR-induced Ca²⁺

SUBMITTER: Morgan AJ 

PROVIDER: S-EPMC5531262 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature