Turner N C, Dollery C T, Williams A J
Department of Clinical Pharmacology, Royal Postgraduate Medical School, Hammersmith Hospital, London, England.
J Cardiovasc Pharmacol. 1989;13 Suppl 5:S180-2. doi: 10.1097/00005344-198900135-00049.
Endothelin-1 (ET-1) produced concentration-dependent contractions of rat aorta and rat trachea. These contractions were dependent on the presence of extracellular calcium but unaffected by nicardipine. Contractions of aorta could be attenuated with the potassium channel activator BRL 34915. BRL 34915 also elicited dose-related relaxations of rat aorta and trachea precontracted with ET-1. We conclude that although the increase in calcium permeability elicited by ET-1 may not involve dihydropyridine-sensitive calcium channels, its reversal by BRL 34915 suggests that smooth muscle contraction by ET-1 may involve a voltage-linked mechanism.
内皮素-1（ET-1）可引起大鼠主动脉和气管产生浓度依赖性收缩。这些收缩依赖于细胞外钙的存在，但不受尼卡地平的影响。主动脉的收缩可被钾通道激活剂BRL 34915减弱。BRL 34915还可引起经ET-1预收缩的大鼠主动脉和气管出现剂量相关的舒张。我们得出结论，尽管ET-1引起的钙通透性增加可能不涉及二氢吡啶敏感的钙通道，但其被BRL 34915逆转表明ET-1引起的平滑肌收缩可能涉及电压相关机制。
