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The protective effect of benidipine hydrochloride, a 1,4-dihydropyridine calcium antagonist, was investigated in cultured mouse fetal heart cells under the hypoxic condition (PO2, &lt; or = 20 mmHg). The preparation of cultured fetal mouse heart muscle cells was subjected to the hypoxic condition for 24 hr. After the hypoxic treatment for 24 hr, the spontaneously beating rate of cultured heart cells was reduced subsequently and the beating almost ceased. Protection against cell injury was assessed by cell viability (NR assay), LDH release and cellular ATP levels. Under the hypoxic condition, cell viability and cellular ATP levels were markedly decreased, and LDH release was increased. Benidipine hydrochloride, at concentrations higher than 1-10 nM, strongly protected against the decreases in cell viability and cellular ATP levels as well as the increase in LDH release. The potency of the protective effect of benidipine hydrochloride was greater than those of the other tested 1,4-dihydropyridine calcium antagonists (nisoldipine, nitrendipine and nifedipine). These results suggest that benidipine hydrochloride exerts protective actions against hypoxic myocardial injury of cultured mouse fetal heart cells.

The protective effect of benidipine hydrochloride against hypoxic myocardial injury of cultured mouse fetal heart cells.