Effects of Ca2+ channel antagonists on acetylcholine and catecholamine releases in the in vivo rat adrenal medulla.
Effects of Ca2+ channel antagonists on acetylcholine and catecholamine releases in the in vivo rat adrenal medulla.
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Ca2 通道拮抗剂对体内大鼠肾上腺髓质乙酰胆碱和儿茶酚胺释放的影响。
DOI：
10.1152/ajpregu.00609.2003
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
K. Sunagawa
中科院分区：
文献类型：
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作者：
T. Akiyama;T. Yamazaki;H. Mori;K. Sunagawa
为了阐明体内肾上腺髓质中控制ACh和儿茶酚胺释放的电压依赖性Ca(2+)通道的类型，我们在麻醉大鼠的左肾上腺髓质中植入微透析探针，并研究Ca(2+)通道拮抗剂对神经刺激诱导的ACh、去甲肾上腺素和肾上腺素释放的影响。透析探针用含有胆碱酯酶抑制剂新斯的明的林格溶液灌注。在静脉内给予Ca(2+)通道拮抗剂之前和之后，以2和4Hz电刺激左内脏神经。 omega-Conotoxin GVIA（一种 N 型 Ca(2+) 通道拮抗剂，10 µg/kg）抑制 2 和 4 Hz 频率下的乙酰胆碱释放约 40%，抑制 4 Hz 频率下去甲肾上腺素释放约 50%，抑制 2 和 4 Hz 频率下肾上腺素释放约 45%。五倍高剂量的 omega-芋螺毒素 GVIA（50 微克/千克）并没有进一步抑制这些释放。 omega-芋螺毒素 MVIIC（一种 P/Q 型 Ca(2+) 通道拮抗剂，50 µg/kg）在 4 Hz 时抑制乙酰胆碱和肾上腺素释放约 30%。联合使用 omega-芋螺毒素 GVIA（50 微克/千克）和 MVIIC（250 微克/千克）可抑制 2 赫兹和 4 赫兹的乙酰胆碱释放约 70%，抑制 2 赫兹和 4 赫兹的去甲肾上腺素和肾上腺素释放约 80%。硝苯地平（一种 L 型 Ca(2+) 通道拮抗剂，300 和 900 µg/kg）不会改变 2 和 4 Hz 时的乙酰胆碱释放；然而，硝苯地平（300微克/千克）在4赫兹时抑制肾上腺素释放20％，硝苯地平（900微克/千克）在4赫兹时抑制去甲肾上腺素和肾上腺素释放30％。总之，N型和P/Q型Ca(2+)通道均控制节前内脏神经末梢的ACh释放，而L型Ca(2+)通道则不然。 L 型 Ca(2+) 通道参与嗜铬细胞上去甲肾上腺素和肾上腺素的释放。
To elucidate the types of voltage-dependent Ca(2+) channels controlling ACh and catecholamine releases in the in vivo adrenal medulla, we implanted microdialysis probes in the left adrenal medulla of anesthetized rats and investigated the effects of Ca(2+) channel antagonists on ACh, norepinephrine, and epinephrine releases induced by nerve stimulation. The dialysis probes were perfused with Ringer solution containing a cholinesterase inhibitor, neostigmine. The left splanchnic nerves were electrically stimulated at 2 and 4 Hz before and after intravenous administration of Ca(2+) channel antagonists. omega-Conotoxin GVIA (an N-type Ca(2+) channel antagonist, 10 microg/kg) inhibited ACh release at 2 and 4 Hz by approximately 40%, norepinephrine release at 4 Hz by approximately 50%, and epinephrine release at 2 and 4 Hz by approximately 45%. A fivefold higher dose of omega-conotoxin GVIA (50 microg/kg) did not further inhibit these releases. omega-Conotoxin MVIIC (a P/Q-type Ca(2+) channel antagonist, 50 microg/kg) inhibited ACh and epinephrine releases at 4 Hz by approximately 30%. Combined omega-conotoxin GVIA (50 microg/kg) and MVIIC (250 microg/kg) inhibited ACh release at 2 and 4 Hz by approximately 70% and norepinephrine and epinephrine releases at 2 and 4 Hz by approximately 80%. Nifedipine (an L-type Ca(2+) channel antagonist, 300 and 900 microg/kg) did not change ACh release at 2 and 4 Hz; however, nifedipine (300 microg/kg) inhibited epinephrine release at 4 Hz by 20%, and nifedipine (900 microg/kg) inhibited norepinephrine and epinephrine releases at 4 Hz by 30%. In conclusion, both N- and P/Q-type Ca(2+) channels control ACh release on preganglionic splanchnic nerve endings while L-type Ca(2+) channels do not. L-type Ca(2+) channels are involved in norepinephrine and epinephrine releases on chromaffin cells.
关于乙酰胆碱或大鼠肾上腺透壁刺激引起的儿茶酚胺分泌的研究。
DOI：
10.1113/jphysiol.1981.sp013676
发表时间：
1981
期刊：
The Journal of physiology
影响因子：
--
作者：
Wakade,AR
通讯作者：
Wakade,AR