Voltage-sensitive release mechanism was pharmacologically dissected from the Ca2⁢-induced Ca2⁢ release in the SR Ca2⁢ release in the rat ventricular myocytes patch-clamped in a whole-cell mode. SR Ca2⁢ release process was monitored by using forward-mode Na⁢-Ca2⁢ exchange after restriction of the interactions between Ca2⁢ from SR and Na⁢-Ca2⁢ exchange within micro-domains with heavy cytosolic Ca2⁢ buffering with 10 mM BAPTA. During stimulation every 10 s with a pulse roughly mimicking action potential, the initial outward current gradually turned into a huge inward current of ⁣12.9⁑0.5 pA/pF. From the inward current, two different inward INCXs were identified. One was 10 μM ryanodine-sensitive, constituting 14.2⁑2.3%. It was completely blocked by CdCl2 (0.1 mM and 0.5 mM) and by Na⁢-depletion. The other was identified by 5 mM NiCl2 after suppression of ICaL and ryanodine receptor, constituting 14.8⁑1.6%. This latter was blocked by either 10 mM caffeine-induced SR Ca2⁢-depletion or 1 mM tetracaine. IV-relationships illustrated that the latter was activated until the peak in 30∼35 mV lower voltages than the former. Overall, it was concluded that the SR Ca2⁢ release process in the rat ventricular myocytes is mediated by the voltage-sensitive release mechanism in addition to the Ca2⁢-induced-Ca2⁢ release.