Ito Y, Kuriyama H, Suzuki H
Br J Pharmacol. 1978 Dec;64(4):503-10. doi: 10.1111/j.1476-5381.1978.tb17311.x.
1 The effects of diltiazem on electrical and mechanical properties of vascular smooth muscles of the rabbit were examined by various experimental procedures. 2 In the pulmonary artery, diltiazem (0.1 to 10 microgram/ml) did not modify the membrane potential (-56 mV), length constant of the tissue (1.47 mm) or rectifying properties of the membrane. Diltiazem (0.1 to 10 microgram/ml) did not modify the membrane potential of the mesenteric artery (-62.5 mV). 3 Diltiazem (1 to 10 microgram/ml) suppressed mechanical responses of pulmonary and mesenteric arteries induced either by direct stimulation of the muscle (1.0 s pulse) or by neural activation (0.5 ms pulse, 30 Hz and 10 s total duration). Diltiazem suppressed the contraction induced by nerve stimulation to a greater extent than that induced by direct muscle stimulation. 4 When the depolarization-contraction relationship of the smooth muscle of the pulmonary artery was observed by voltage clamp technique, diltiazem (1 to 10 microgram/ml) raised the critical membrane potential to evoke contraction from 5 mV to 12 mV, and reduced the amplitude of contraction obtained at any given depolarization level. 5 In the pulmonary artery, diltiazem (10 microgram/ml) suppressed K-induced contraction and raised the mechanical threshold, while K-induced depolarization was not suppressed. Diltiazem (1 to 10 microgram/ml) also suppressed noradrenaline-induced contraction, raised the mechanical threshold and suppressed noradrenaline-induced depolarization. 6 The vasodilator actions of diltiazem on the vascular smooth muscle were compared to vasodilator actions observed with other Ca-antagonists.
1 通过各种实验方法研究了地尔硫䓬对兔血管平滑肌电生理和机械特性的影响。2 在肺动脉中，地尔硫䓬（0.1至10微克/毫升）未改变膜电位（-56毫伏）、组织的长度常数（1.47毫米）或膜的整流特性。地尔硫䓬（0.1至10微克/毫升）未改变肠系膜动脉的膜电位（-62.5毫伏）。3 地尔硫䓬（1至10微克/毫升）抑制了肺动脉和肠系膜动脉由直接刺激肌肉（1.0秒脉冲）或神经激活（0.5毫秒脉冲，30赫兹，总持续时间10秒）所诱导的机械反应。地尔硫䓬对神经刺激诱导的收缩的抑制作用比对直接肌肉刺激诱导的收缩的抑制作用更大。4 当通过电压钳技术观察肺动脉平滑肌的去极化-收缩关系时，地尔硫䓬（1至10微克/毫升）将诱发收缩的临界膜电位从5毫伏提高到12毫伏，并降低了在任何给定去极化水平下获得的收缩幅度。5 在肺动脉中，地尔硫䓬（10微克/毫升）抑制钾诱导的收缩并提高机械阈值，而钾诱导的去极化未被抑制。地尔硫䓬（1至10微克/毫升）也抑制去甲肾上腺素诱导的收缩，提高机械阈值并抑制去甲肾上腺素诱导的去极化。6 将地尔硫䓬对血管平滑肌的舒张作用与其他钙拮抗剂所观察到的舒张作用进行了比较。
