Friedman D J, Duckles S P
Department of Pharmacology, College of Medicine, University of California, Irvine 92717.
Life Sci. 1994;54(21):1545-57. doi: 10.1016/0024-3205(94)90025-6.
Influx of calcium through voltage-dependent N-type calcium channels promotes the release of norepinephrine from nerve terminals. Contributions by L- and N-type calcium channels at different levels of nerve stimulation were examined in perfused rat tail arteries loaded with [3H]norepinephrine. Nifedipine had no effect while omega-conotoxin reduced tritium efflux by 69 to 82% depending on the stimulation intensity. Thus, N-type calcium channels predominated in the control of norepinephrine release, and the relative contribution of L- and N-type channels did not change when stimulation intensity was altered. We also explored the effect of calcium channel blockers on modulation of norepinephrine release by D2 dopamine receptors. Inhibition of stimulation-evoked tritium efflux by the D2 agonist N-0923 was similar in the absence and presence of nifedipine and/or omega-conotoxin. We conclude that D2 dopamine receptors are not coupled to L-type calcium channels; however, the role of N-type calcium channels requires further investigation.
通过电压依赖性N型钙通道的钙内流促进去甲肾上腺素从神经末梢释放。在装载有[3H]去甲肾上腺素的灌注大鼠尾动脉中，研究了L型和N型钙通道在不同神经刺激水平下的作用。硝苯地平无作用，而ω-芋螺毒素根据刺激强度使氚外流减少69%至82%。因此，N型钙通道在去甲肾上腺素释放的控制中占主导地位，当刺激强度改变时，L型和N型通道的相对作用没有变化。我们还探讨了钙通道阻滞剂对D2多巴胺受体调节去甲肾上腺素释放的影响。在不存在和存在硝苯地平和/或ω-芋螺毒素的情况下，D2激动剂N-0923对刺激诱发的氚外流的抑制作用相似。我们得出结论，D2多巴胺受体不与L型钙通道偶联；然而，N型钙通道的作用需要进一步研究。
