Usui H, Akimoto Y, Kurahashi K, Shirahase H, Fujiwara M, Shibata S, Suzuki A
Department of Pharmacology, Faculty of Medicine, Kyoto University, Japan.
Jpn J Pharmacol. 1990 Oct;54(2):237-40. doi: 10.1254/jjp.54.237.
The stable thromboxane A2 analogue, STA2, caused concentration-dependent contractions in the canine basilar artery. In Ca2(+)-free medium containing EGTA (0.1 mM) and nifedipine (10(-6) M), the addition of Ca2+ (2.5 mM) in the presence of STA2 (10(-8) M) caused a tonic contraction (nifedipine-resistant Ca2(+)-induced contraction). In the basilar artery, nitroglycerin did not significantly affect such nifedipine-resistant Ca2(+)-induced contractions, but nearly abolished the contraction in the coronary artery. The present experiments suggest that the regulatory mechanism of mobilized Ca2+ for the nifedipine-resistant Ca2(+)-induced contraction produced by STA2 in the basilar artery is different from that in the coronary artery.
稳定的血栓素A2类似物STA2可引起犬基底动脉浓度依赖性收缩。在含有EGTA(0.1 mM)和硝苯地平(10^(-6) M)的无钙培养基中,在STA2(10^(-8) M)存在的情况下添加Ca2+(2.5 mM)会引起强直性收缩(硝苯地平抵抗性Ca2+诱导的收缩)。在基底动脉中,硝酸甘油对这种硝苯地平抵抗性Ca2+诱导的收缩没有显著影响,但几乎完全消除了冠状动脉中的收缩。本实验表明,STA2在基底动脉中产生的硝苯地平抵抗性Ca2+诱导收缩所涉及的动员Ca2+的调节机制与冠状动脉中的不同。