Casteels R, Login I S
J Physiol. 1983 Jul;340:403-14. doi: 10.1113/jphysiol.1983.sp014769.
The effects of reserpine on excitation-contraction coupling and 45Ca exchange of smooth muscle cells of the rabbit ear artery and the guinea-pig taenia coli have been studied. Reserpine inhibited the spontaneous mechanical activity of the taenia coli and the force development induced by 59 mM-external K or 10(-5) M-carbachol. In the ear artery reserpine blocked the K-induced contraction but its effect on the contraction elicited by noradrenaline was smaller. At 0.2 mM-Ca, the inhibition of the tonic component of the noradrenaline-induced contraction was more pronounced than that of the phasic component. This reserpine action was fully reversible for the noradrenaline stimulus in the ear artery but less so for K-induced contractions. The inhibitory action on contractions induced in taenia coli by K-rich solution and by carbachol was even less reversible. The analysis of the effect of reserpine on the 45Ca exchange in the ear artery has revealed that it inhibits the increase of the fractional loss induced by K depolarization, but that it does not exert a significant effect on the increased fractional loss induced by 10(-5) M-noradrenaline. Reserpine slows down the filling with 45Ca of the agonist-sensitive store without affecting the steady-state amount of Ca taken up by the store. A study of the degree of filling of the store by measuring the force development and the 45Ca release elicited by noradrenaline in Ca-free medium, reveals that the force development after loading in a reserpine-containing medium remains less than the control, although the same amount of Ca is released from the store. It was shown by using tetrabenazine that the inhibitory action of reserpine on the Ca exchange and the force development is not due to an interaction of reserpine with the receptor molecules that are responsible for its depleting action on aminergic granules. These results strongly suggest that reserpine exerts a Ca antagonistic action on smooth muscle whereby it blocks the potential-dependent channels. However, reserpine also affects the receptor-operated channels to some extent and in addition at a high concentration it seems to exert an unspecific inhibitory action on the contractile system.
已对利血平对兔耳动脉和平滑肌细胞的兴奋 - 收缩偶联及45Ca交换的影响进行了研究。利血平抑制了结肠带的自发机械活动以及由59 mM细胞外钾或10(-5) M卡巴胆碱诱导的张力发展。在耳动脉中，利血平阻断了钾诱导的收缩，但其对去甲肾上腺素诱导的收缩的作用较小。在0.2 mM钙时，利血平对去甲肾上腺素诱导收缩的强直成分的抑制比对相性成分的抑制更明显。利血平对耳动脉中去甲肾上腺素刺激的这种作用是完全可逆的，但对钾诱导的收缩则不然。其对结肠带中富钾溶液和卡巴胆碱诱导的收缩的抑制作用甚至更不可逆。对利血平对耳动脉中45Ca交换的影响分析表明，它抑制了钾去极化诱导的分数丢失增加，但对10(-5) M去甲肾上腺素诱导的分数丢失增加没有显著影响。利血平减缓了激动剂敏感储存库中45Ca的填充，而不影响储存库摄取的钙的稳态量。通过测量去甲肾上腺素在无钙培养基中诱导的张力发展和45Ca释放来研究储存库的填充程度，结果表明，尽管从储存库中释放出相同量的钙，但在含利血平的培养基中加载后产生的张力仍低于对照。使用丁苯那嗪表明，利血平对钙交换和张力发展的抑制作用不是由于利血平与负责其对胺能颗粒耗竭作用的受体分子相互作用所致。这些结果强烈表明，利血平对平滑肌发挥钙拮抗作用，从而阻断电位依赖性通道。然而，利血平在一定程度上也影响受体操纵通道，此外，在高浓度时，它似乎对收缩系统发挥非特异性抑制作用。
