Satoh H
Department of Pharmacology, Nara Medical University, Kashihara, Japan.
Eur J Pharmacol. 1998 Apr 10;346(2-3):309-13. doi: 10.1016/s0014-2999(98)00048-x.
Effects of taurine on the inwardly rectifying K+ current (IK1) in isolated guinea pig ventricular cardiomyocytes were examined using patch voltage-clamp methods. All experiments were performed at 36 degrees C. Taurine (10-20 mM) increased the action potential duration, but failed to affect the resting potential. Holding potential was maintained at -30 mV. The current was activated with an inwardly going rectification, and was completely blocked by Ba2+ (2 mM). Taurine inhibited IK1 at - 120 mV by 28.3+/-1.1% (n=6, P < 0.05) at 10 mM and by 36.0+/-2.1% (n=6, P < 0.01) at 20 mM. The reversal potential was shifted in the hyperpolarizing direction by 3.7+/-0.6 mV (n=6) at 20 mM. In inside-out patch-clamp experiments, the amplitude of unitary channels was -2.7+/-0.3 pA (n=21) at -90 mV. Symmetrical high-K+ (150 mM) solutions in both bath and pipette were used. The channel conductance was 32+/-2 pS (n=9). Taurine did not affect channel conductance, but markedly decreased the open probability at - 120 mV of channel by 21.5+/-2.4% (n=8, P < 0.01) at 10 mM, and by 56.7+/-3.8% (n=8, P < 0.001) at 20 mM. These responses were almost reversible. These results suggest that taurine directly modulates the open probability of the inwardly rectifying K+ current, resulting in regulation of the functions of heart cells.
采用膜片钳电压钳技术，研究了牛磺酸对豚鼠离体心室肌细胞内向整流钾电流（IK1）的影响。所有实验均在36℃下进行。牛磺酸（10 - 20 mM）可延长动作电位时程，但对静息电位无影响。钳制电位保持在 - 30 mV。该电流通过内向整流被激活，并被2 mM Ba2+完全阻断。在 - 120 mV时，10 mM牛磺酸使IK1抑制28.3±1.1%（n = 6，P < 0.05），20 mM牛磺酸使IK1抑制36.0±2.1%（n = 6，P < 0.01）。在20 mM时，反转电位向超极化方向偏移3.7±0.6 mV（n = 6）。在内外膜片钳实验中，在 - 90 mV时，单通道电流幅度为 - 2.7±0.3 pA（n = 21）。浴槽液和微电极内液均采用对称的高钾（150 mM）溶液。通道电导为32±2 pS（n = 9）。牛磺酸不影响通道电导，但在 - 120 mV时，10 mM牛磺酸可使通道开放概率显著降低21.5±2.4%（n = 8，P < 0.01），20 mM牛磺酸可使通道开放概率显著降低56.7±3.8%（n = 8，P < 0.001）。这些反应几乎是可逆的。这些结果表明，牛磺酸直接调节内向整流钾电流的开放概率，从而调节心脏细胞的功能。
