Ca²⁺channel blockers with dihydropyridine structure, which block the L-type Ca²⁺ channel, are widely used against hypertension and angina. Addition of blocking activities against other types of Ca²⁺ channels such as the T-type Ca²⁺ channel, would lead to bradycardiac effects on the isolated cardiac pacemaker, and reduction of reflex tachycardia when applied in vivo.　Excellent clinical profiles of these drugs such as cardioprotective and renal protective effects have been reported. Structural modification of these compounds will provide specific T-type Ca²⁺ channel blockers which may be useful in research and in therapy. Some dihydropyridine compounds such as AHC-52 do not block　the L-type Ca²⁺ channel, but block the cAMP-activated Cl^- channel. These compounds enhance the recovery of myocardial contractile force after experimental ischemia-reperfusion. Unlike the well-known cardioprotective agents acting through modification of cation homeostasis such as b blockers, Ca²⁺ channel blockers and K⁺ channel openers, the Cl^- channel blocking dihydropyridines do not influence myocardial contractile force during normoxia. In the future, dihydropyridines with different balance of inhibitory effects against various ion channels may be developed as novel therapeutic agents