中文摘要：

血管平滑肌细胞膜上存在氯离子通道，不仅参与调节平滑肌细胞的肌原性紧张，而且参与多种血管床的神经平滑肌细胞之间的信息传递，但氯离子通道及其阻断剂对耳蜗螺旋动脉（spiral modiol arartery，SMA）平滑肌细胞兴奋性接头电位（excitatory junction potential，EJP）是否有影响，尚不清楚。本实验运用细胞内微电极记录技术，在豚鼠耳蜗SMA离体标本上，研究氯通道阻断剂（niflumic acid，NFA,indanyloxyacetic acid 94，IAA-94；disodium 4，4’-diisothiocyanatostilbene-2．2’-disulfonate，DIDS）对去甲肾上腺素（norepinephrine，NE）引起SMA平滑肌细胞去极化反应和平滑肌细胞EJP的影响。结果显示，多数SMA平滑肌细胞在适宜的刺激下，通过神经兴奋传递产生EJP（75％，n=49）。在联合使用α1（prazosin，0．1-1 μmol／L），α2（idazoxan，0．3-1μmol／L）和P2x（PPADS，10-100μmol／L）受体拮抗剂时，所产生的EJP幅值仅有30％-80％被抑制。在使用上述拮抗剂的基础上，NFA（10-1000μmol/L）能进一步抑制EJP，而且缩短EJP的时程。减少细胞外氯离子浓度（由135．6mmol／L减少到60mmol／L），在同样刺激强度下激起的EJP的幅度和时程均增加，低氯的这一作用可被IAA-94和DIDS所反转。NFA和IAA-94也可进一步抑制α1、α2和β受体拮抗剂联合使用不能消除的NE（1—50μmol／L）引起的去极化反应。结果提示：NE可能通过激活一类非α、非β肾上腺能受体（可能属于γ肾上腺能受体）引起氯离子通道开放，增加氯离子电导，调节耳蜗SMA平滑肌细胞的生理活动。

英文摘要：

Chloride channels have been identified in vascular smooth muscle cells （SMCs）. It has been shown that these channels are involved in myogenic tone regulation and neuromuscular transmission in various vascular beds. However, whether the chloride channels are responsible for the formation of excitatory junction potentials （EJPs） of SMCs in the spiral modiolar artery （SMA） remains unelucidated. In the present study, the effects of chloride channel blockers （niflumic acid, NFA; indanyloxyacetic acid 94, IAA-94; disodium 4,4＇-diisothiocyanatostilbene-2,2＇-disulfonate, DIDS） on EJP were explored in guinea pigs, using intracellular recording techniques on acutely isolated SMA. It was found that EJP was evoked in the majority of the SMCs （75%, n=49） with an adequate electronic stimulation. The amplitude of the EJP was partially blocked （30%-80%） by combined application of α1 receptor antagonist （prazosin） and α2 receptor antagonist （idazoxan） at concentration of up to 1 μmol/L, and P2x receptor antagonist （PPADS, 10-100 μmol/L）.NFA （100 μmol/L） could further inhibit the residual EJP in the presence of α1,α2-adrenergic and P2x receptor antagonists. IAA-94 or DIDS not only inhibited the amplitude but also shortened the duration of EJP. Decrease of extracellular chloride concentration from 135.6 mmol/L to 60 mmol/L would enhance EJP. Moreover, IAA-94 （100 μmol/L） and DIDS （200 μmol/L） could reverse the enhancement of FJP by low extracellular Cl^-. NFA （100 μmol/L） could also block the residual depolarizations evoked by norepinephrine （NE, 1-50μmol/L）. Based on these results, it is inferred that NE could activate a novel adrenoceptor to open the chloride channel on the membrane of the SMCs, leading to a transmembrane Cl^- current. This current is involved, at least partially, in the formation of EJP.