硝苯吡啶抑制豚鼠交感神经元的钙依赖性电位

NIFEDIPINE INHIBITS CALCIUM-DEPENDENT POTENTIALS IN GUINEA PIG SYMPATHETIC NEURONS

应用细胞内记录技术观察了钙通道阻滞剂硝苯吡啶(nifedlpine)对离体豚鼠腹腔神经节细胞三种钙依赖性电位的可逆性作用。硝苯吡啶(0.1—1mmol/L)可剂量依赖式地抑制动作电位后超极化、强直后膜电位的变化,在无钠高钙加 TEA 溶液中,硝苯吡啶(0.1μmol/L)能抑制钙锋电位。结果表明,大剂量的硝苯吡啶可继发性抑制钙依赖性钾电导,临床治疗剂量的硝苯吡啶还直接减少钙电导。以上作用是硝苯吡啶调节交感节后神经元的兴奋性,阻滞突触前膜 ACh 的量子性释放的基础。

Reversible effects of nifedipine,a calcium channel blocker,on 3 types of calcium-dependent potentials in the celiac ganglion cells of the guinea pigs in vitro wereinvestigated by means ofintracellular recordings.Nifedipine(0.1—1 mmool/L)inhibited the spike afterhyperpolarization,thepost-tetanic membrane potential in dose-dependent manner Nifedipine(0.1μmol/L)also depressed the Ca^(2+)spike potential in a Na^+-free/high Ca^(2+)solutionplus TEA.Thus the resalts indicate that nifedipine in clinical theuraputicdosage may directly reduce Ca^(2+) conductance and then in higher concentration mayalso depress secondarily Ca^(2+)dependent potassium conductance.These actions ofnifedipine may underlie the mechanism of blockade of quantal release of ACh frompresynaptic membrane as well as the modulation of excitability of sympatheticpostganglionic neuron.