Küçükhüseyin C, Silan C
Department of Pharmacology, Cerrahpaşa Medical Faculty, University of Istanbul, Turkey.
J Basic Clin Physiol Pharmacol. 1997;8(1-2):81-9. doi: 10.1515/jbcpp.1997.8.1-2.81.
Exposure of guinea-pig papillary muscle to 22 mM K+ resulted in loss of electromechanical excitability accompanied by an elevation of mean electrical threshold by 8.96 V and a membrane depolarization of about 47.3 mV. After setting the threshold to a new sensitive level for stimulation, 4-AP (1.25-5 x 10(-3) M) could restore both the propagated action potentials typical for Ca2+ (e.g. resting potential: -46 mV; action potential amplitude: 74.25 mV; upstroke velocity: 11.4 V/sec; abolition by Ca(2+)-channel blokers) and contractions to papillary muscle cells, with further elevation of resting potential from -51.2 mV to -46 mV. Restoration of electromechanical activity by 4-AP was dose-dependent and susceptible to blockade with D600 (5 x 10(-7) M). From these data, it was concluded that 4-AP restored electrical and mechanical excitability by increasing membrane conductance to Ca2+ (gCa2+).
将豚鼠乳头肌暴露于22 mM K+会导致机电兴奋性丧失，同时平均电阈值升高8.96 V，膜去极化约47.3 mV。在将阈值设定为新的敏感刺激水平后，4-氨基吡啶（4-AP，1.25 - 5×10⁻³ M）可恢复乳头肌细胞典型的Ca²⁺传播动作电位（例如静息电位：-46 mV；动作电位幅度：74.25 mV；上升速度：11.4 V/秒；被Ca²⁺通道阻滞剂消除）和收缩，静息电位进一步从-51.2 mV升高到-46 mV。4-AP对机电活性的恢复呈剂量依赖性，且易被D600（5×10⁻⁷ M）阻断。根据这些数据得出结论，4-AP通过增加膜对Ca²⁺的电导（gCa²⁺）来恢复电和机械兴奋性。
