SUMMARY AHC‐52 is a dihydropyridine compound known to reverse multidrug resistance through inhibition of the P‐glycoprotein. In whole‐cell voltage‐clamped cardiomyocytes, AHC‐52 had no effect on L‐type calcium current but inhibited cAMP‐activated chloride current. In an ischemia‐reperfusion model with coronary‐perfused right ventricular tissue, AHC‐52 markedly enhanced the recovery of contractile force on reperfusion without any negative inotropic effect during normal perfusion and experimental ischemia, which is similar to the effects of chloride blockers such as 9‐anthracenecarboxylic acid (9AC) and 4‐acetamido‐4′isothiocyanostilbene‐2,2 disulfonic acid (SITS). Thus, AHC‐52 appears to be an interesting prototype of cardioprotective drugs acting through mechanisms related to modification of anion homeostasis.
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Tanaka et al. (2000) studied this question.
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