中文摘要：

本文旨在观察钙激活氯通道（calcium-activated Cl^- channels, CaCCs）在大鼠脑基底动脉舒缩活动中的作用。应用压力肌动图技术观察给予不同药物干预后大鼠脑基底动脉血管段直径的变化。结果显示：（1）脑基底动脉管腔内压力为0-100 mmHg时，压力诱发引起的脑血管舒缩活动的比例为78.6% （n = 28），且血管的收缩比舒张反应更快。（2）脑基底动脉管腔内压力为60 mmHg时，振幅平均值为（62.6 ± 6.4） μm （n = 22），频率平均为（8.0 ± 2.3） 次/5 min （n = 22）。（3）在细胞外液无钙时，血管段舒缩活动减弱。（4）在细胞外液加入L-型钙通道阻断剂尼莫地平，血管段舒缩活动减弱。（5）在细胞外液加入CaCCs通道阻断剂尼氟灭酸（niflumic acid, NFA）和NPPB [5-nitro-2-（3-phenylpropylamine）benzoic acid]，压力诱发的血管舒缩活动减弱，并使脑基底动脉血管保持持续舒张。以上结果提示，管腔内压力诱发的脑基底动脉血管舒缩活动与细胞外钙内流及CaCCs作用相关。

英文摘要：

This study investigated the role of calcium-activated Cl^- channels （CaCCs） in mediating vasomotor activity of cerebral basilar artery （BA） of Wistar rat. Pressure myograph was used to examine the changes in diameter of isolated BA to vasoactive reagents. The results showed that （1） The rate of pressure-induced vasomotor activity was 78.6% （n = 28） in BA from 0 to 100 mmHg working pressure. The contractile phase of the response was faster than the relaxation phase; （2） The amplitude of contraction was （62.6 ± 6.4） μm （n = 22）, the frequency of contraction was variable and the highest value was 8.0 ± 2.3 per 5 min at 60 mmHg working pressure （n = 22）; （3） The pressure-induced vasomotor activity of BA was markedly attenuated when Ca^2＋ was removed from medium; （4） The pressure-induced vasomotor activity was blocked by voltage dependent Ca^2＋ channel blocker nimodipine; （5） The pressure-induced vasomotor was inhibited by CaCC antagonists NFA and NPPB. These results suggest that the pressure-induced vasomotor activity of isolated BA is associated with Ca2＋ influx that activates CaCCs.