Yokotani K, Okuma Y, Osumi Y
Department of Pharmacology, Kochi Medical School, Nankoku, Japan.
Jpn J Pharmacol. 1998 Sep;78(1):75-7. doi: 10.1254/jjp.78.75.
We characterized the voltage-activated Ca2+ channels involved in noradrenaline (NA) release from gastric sympathetic neurons using isolated, vascularly perfused rat stomach. The evoked NA release by electrical stimulation of periarterial nerves was abolished by calcium removal from the perfusion medium and by cadmium. Omega-conotoxin GVIA (N-type Ca2+-channel blocker) effectively and omega-conotoxin MVIIC (N/P/Q-type blocker) slightly inhibited the evoked NA, while omega-agatoxin IVA (P-type blocker) had no effect. These results suggest that omega-conotoxin GVIA and omega-conotoxin MVIIC-sensitive N-type Ca2+ channels are involved in NA release from the rat gastric sympathetic nerve terminals.
我们使用分离的、经血管灌注的大鼠胃,对参与胃交感神经元去甲肾上腺素(NA)释放的电压激活Ca2+通道进行了表征。通过从灌注介质中去除钙和使用镉,可消除动脉周围神经电刺激诱发的NA释放。ω-芋螺毒素GVIA(N型Ca2+通道阻滞剂)有效,而ω-芋螺毒素MVIIC(N/P/Q型阻滞剂)轻微抑制诱发的NA释放,而ω-阿加毒素IVA(P型阻滞剂)则无作用。这些结果表明,ω-芋螺毒素GVIA和对ω-芋螺毒素MVIIC敏感的N型Ca2+通道参与大鼠胃交感神经末梢的NA释放。