Opening of the ATP-dependent K-channels (KATP channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective KATP channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial KATP channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoKATP channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoKATP channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoKATP channels increases the cardiac electrical stability in rats with PIC.
|Number of pages||4|
|Journal||Eksperimental'naya i Klinicheskaya Farmakologiya|
|Publication status||Published - 2004|
ASJC Scopus subject areas
- Pharmacology, Toxicology and Pharmaceutics(all)