Cardioprotective effect against ischemia-reperfusion injury of AHC-52, a dihydropyridine compound with inhibitory effect on Cl- but not Ca2+ current.

We examined the effects of a dihydropyridine compound, AHC-52, on guinea pig myocardium. In ventricular cardiomyocytes, AHC-52 (1 microM) had no effect on the basal peak inward and steady state currents, but inhibited the isoprenaline-induced time independent Cl- current. In coronary perfused right ventricular preparations, no-flow ischemia induced decreases in developed tension which recovered only to about 50% of initial values after reperfusion. AHC-52 (0.1 microM) had no effect on developed tension under normal conditions and during ischemia, but significantly improved the recovery of developed tension after reperfusion to about 80% of preischemic values. Thus, AHC-52 inhibits Cl- channels in cardiac muscle and may have protective effects against ischemia-reperfusion injury.