Mras S, Sperelakis N
Eur J Pharmacol. 1981 Apr 24;71(1):13-9. doi: 10.1016/0014-2999(81)90382-4.
Reaggregate cultures (primary) were prepared from enzyme-dispersed vascular smooth muscle (VSM) cells from rat aortas. The cultures were incubated for 7-10 days, and then studied by the intracellular microelectrode technique. The cells were electrically quiescent (mean resting potential of --47 mV), and extracellular electrical stimulation usually did not elicit a membrane response. Addition of 10 mM tetraethylammonium rapidly induced excitability, allowing the VSM cells to fire Ca2+-dependent action potentials in response to electrical stimulation. The electrical responses often had two components, an initial spike and a later plateau-like component. The action potential spikes had a mean amplitude of 22 mV but occasionally were overshooting; the plateaus had a mean duration (at 50% repolarization) of 3.8 sec. A new anti-anginal agent, bepridil (10(-8)-10(-5) M), depressed the amplitude and duration of the plateau and blocked the spike component of the action potential in a dose-dependent fashion without affecting the resting potential. This finding is consistent with the view that bepridil acts as a Ca2+-antagonistic agent to prevent the generation of the action potentials, and this action can explain its antianginal properties.
重聚集培养物（原代）由大鼠主动脉酶分散的血管平滑肌（VSM）细胞制备而成。将培养物孵育7 - 10天，然后采用细胞内微电极技术进行研究。细胞处于电静息状态（平均静息电位为 - 47 mV），细胞外电刺激通常不会引发膜反应。加入10 mM四乙铵可迅速诱导兴奋性，使VSM细胞在电刺激下产生依赖Ca2 +的动作电位。电反应通常有两个成分，一个初始尖峰和一个随后的平台样成分。动作电位尖峰的平均幅度为22 mV，但偶尔会出现超射；平台的平均持续时间（在复极化50%时）为3.8秒。一种新的抗心绞痛药物苄普地尔（10(-8)-10(-5) M）以剂量依赖性方式降低平台的幅度和持续时间，并阻断动作电位的尖峰成分，而不影响静息电位。这一发现与苄普地尔作为Ca2 +拮抗剂阻止动作电位产生的观点一致，并且这种作用可以解释其抗心绞痛特性。
