Ito H, Sakanashi M, Kawamura T, Nishi K
Arch Int Pharmacodyn Ther. 1984 Sep;271(1):53-63.
The effects of Ca2+-antagonists, diltiazem, verapamil and nifedipine on excised and superfused nodose ganglia of the rabbit were investigated with intracellular recording techniques. In a Na-free solution, somata of nodose ganglion C-cells were capable of eliciting Ca-spikes which were maintained by a Ca-influx when stimulated by passing currents. At a concentration of 10(-5) M, spike amplitude was inhibited to 24% of control by diltiazem, to 16% by verapamil, and to 13% by nifedipine. In a normal physiological solution, diltiazem at 10(-6) M, verapamil at 10(-6) M, and nifedipine at 10(-7) M reduced the maximal rate of rise and at 10(-7) M produced a reduction of the maximal rate of fall of the action potentials accompanied with a prolonged duration, although the resting membrane potential and the amplitude of the action potentials were not altered. The results reveal membrane characteristics of ganglion cells and suggest that Ca2+-antagonists depress not only Ca-influx but also Na-influx and K-efflux.
采用细胞内记录技术,研究了钙离子拮抗剂地尔硫卓、维拉帕米和硝苯地平对家兔离体灌流结节神经节的影响。在无钠溶液中,结节神经节C细胞的胞体在通过电流刺激时能够引发钙峰,该钙峰由钙内流维持。在10⁻⁵M的浓度下,地尔硫卓将峰电位幅度抑制至对照的24%,维拉帕米抑制至16%,硝苯地平抑制至13%。在正常生理溶液中,10⁻⁶M的地尔硫卓、10⁻⁶M的维拉帕米和10⁻⁷M的硝苯地平降低了动作电位的最大上升速率,而在10⁻⁷M时则降低了动作电位的最大下降速率,同时动作电位时程延长,尽管静息膜电位和动作电位幅度未改变。结果揭示了神经节细胞的膜特性,并表明钙离子拮抗剂不仅抑制钙内流,还抑制钠内流和钾外流。