Effects of taurine on L-type voltage-dependent Ca2+ channel in rat cardiomyocytes infected with coxsackievirus B3
Abstract
AIM: To study the effects of taurine on L-type voltage-dependent Ca2+ channel (VDCC) in adult rat cardiomyocytes infected with coxsackievirus B3 (CVB3). METHODS: Whole-cell Ca2+ current of L-type VDCC was obtained by patch-clamp techniques.
RESULTS: The density of L-type Ca2+ current was 4.1 +/- 0.8 pA/pF in normal cardiomyocytes, but increased to 4.9 +/- 1.4 pA/pF with CVB3 infection. At 16 mmol.L-1, taurine decreased the density to 3.5 +/- 0.5 pA/pF in normal cardiomyocytes, and to 3.8 +/- 0.8 pA/pF in CVB3-infected cardiomyocytes. In addition, CVB3 shifted the membrane potential depolarizing to peak current (Vp) from 8 +/- 8 mV to 5 +/- 3 mV which could also be reverted to 8 +/- 4 mV by taurine. CONCLUSION: Taurine inhibited the increase of Ca2+ inflow through L-type VDCC and normalized the decreased Vp induced by CVB3 infection. The effect of taurine on L-type VDCC was the mechanism of taurine attenuating the intracellular Ca2+ accumulation and abnormal electric activities induced by CVB3 infection.
Keywords:
RESULTS: The density of L-type Ca2+ current was 4.1 +/- 0.8 pA/pF in normal cardiomyocytes, but increased to 4.9 +/- 1.4 pA/pF with CVB3 infection. At 16 mmol.L-1, taurine decreased the density to 3.5 +/- 0.5 pA/pF in normal cardiomyocytes, and to 3.8 +/- 0.8 pA/pF in CVB3-infected cardiomyocytes. In addition, CVB3 shifted the membrane potential depolarizing to peak current (Vp) from 8 +/- 8 mV to 5 +/- 3 mV which could also be reverted to 8 +/- 4 mV by taurine. CONCLUSION: Taurine inhibited the increase of Ca2+ inflow through L-type VDCC and normalized the decreased Vp induced by CVB3 infection. The effect of taurine on L-type VDCC was the mechanism of taurine attenuating the intracellular Ca2+ accumulation and abnormal electric activities induced by CVB3 infection.