Kohrogi H, Horio S, Ando M, Sugimoto M, Honda I, Araki S
Am Rev Respir Dis. 1985 Aug;132(2):299-304. doi: 10.1164/arrd.1985.132.2.299.
The effects of nifedipine, a calcium channel blocker, on human bronchial smooth muscle contractions induced by leukotrienes C4 and D4 (LTC4, LTD4), prostaglandin F2 alpha (PGF2 alpha), and potassium were studied in vitro. The LTC4, LTD4, PGF2 alpha, and potassium caused bronchial smooth muscle contractions. After incubation with nifedipine at 2.9 X 10(-6)M, the contractions caused by LTC4, LTD4, PGF2 alpha, and potassium were significantly decreased. Nifedipine also significantly reversed human bronchial smooth muscle contractions previously initiated by these agonists. The effect of nifedipine on potassium contraction was significantly greater than that on LTC4, LTD4, and PGF2 alpha-induced contractions. The pharmacologic feature of nifedipine is that it inhibits the calcium influx associated with membrane depolarization. Therefore, these results suggest that there are two mechanisms of calcium movements in human bronchial smooth muscle contractions induced by LTC4, LTD4, and PGF2 alpha: membrane-depolarization-dependent and -independent mechanisms.
在体外研究了钙通道阻滞剂硝苯地平对由白三烯C4和D4（LTC4、LTD4）、前列腺素F2α（PGF2α）和钾诱导的人支气管平滑肌收缩的影响。LTC4、LTD4、PGF2α和钾会引起支气管平滑肌收缩。在2.9×10⁻⁶M的硝苯地平中孵育后，由LTC4、LTD4、PGF2α和钾引起的收缩显著降低。硝苯地平还能显著逆转先前由这些激动剂引发的人支气管平滑肌收缩。硝苯地平对钾收缩的作用明显大于对LTC4、LTD4和PGF2α诱导收缩的作用。硝苯地平的药理特性是它抑制与膜去极化相关的钙内流。因此，这些结果表明，在由LTC4、LTD4和PGF2α诱导的人支气管平滑肌收缩中，钙运动有两种机制：依赖膜去极化的机制和不依赖膜去极化的机制。
