硝苯吡啶对腹腔神经节突触传递的阻断作用

本文应用细胞内记录技术，观察了钙通道阻滞剂硝苯吡啶（nifedipine)对离体豚鼠腹腔神经节突触传递的影响，硝苯吡啶（0.1-10umol/L)不影响所检细胞的静息膜电位，膜电阻及细胞内刺激引起的动作电位，但能显著阻断N-型胆碱能的突触传递，并且这种作用可被低钙模拟、高钙拮抗，硝苯吡啶（10umol/L)也不影响突触后膜对乙酰胆碱（ACh)的敏感性；但在高钾克氏液中，能减少微小兴奋性突触后电位（mEPSPs)的频率；在低钙和高镁克氏液中，能减少量子含量，而对量子大小无影响。结果表明，治疗量的硝苯吡啶(0.1umol/L)通过阻滞突触前膜钙内流及ACh的量子性释放，产生突触阻断作用。这可能是硝苯吡啶降压机理的一个组成部分。

DEPRESSANT EFFECT OF NIFEDIPINE ON SYNAPTIC TRANSMISSION IN CELIAC GANGLION

The effect of nifedipine, a calcium channel blocker, on nicotinic transmission, was studied in the isolated celiac ganglia of the guinea pig by means of intracellular recordings. Nifedipine in concentration of 0.1-10 mumol/L did not affect resting membrane potential, input membrane resistance and action potential induced by intracellular stimulation in all cells tested, but obviously inhibited nicotinic transmission. The depressant effect of nifedipine on synaptic transmission could be limited by low Ca2+ and antagonized by high Ca2+. Nifedipine did not affect acetylcholine (ACh) sensitivity of postsynaptic membrane, but decreased frequency of miniature excitatory postsynaptic potentials (mEPSPs) in high K+ Kreb's solution and reduced quantal content without effect on quantal size of evoked EPSPs in low Ca2+ /high Mg2+ kreb's solution. The results indicate that nifedipine in therapeutic dose exerts depressant effect on synaptic transmission through blocking Ca2+ entry into presynaptic membrane and reducing quantal release of ACh from presynaptic nerve terminals.