ISSN 0371-0874, CN 31-1352/Q

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生理学报 2006; 58(5): 456-462

氯离子通道阻断剂对豚鼠耳蜗螺旋动脉平滑肌细胞兴奋性接头电位的影响

王英姿, 刘政江, 李丽, 范平, 司军强, 赵磊, 马克涛, 祝丽, 高维建

石河子大学医学院民族高发病与地方病教育部重点实验室电生理研究室，石河子 832002； 武汉大学基础医学院生理学系，武汉 430071； 新疆医科大学第一附属医院，乌鲁木齐 830054

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 modiolar artery, 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a1 (prazosin, 0.1~1 μmol/L)，a2 (idazoxan, 0.3~1 μmol/L)和P2x (PPADS, 10~100 μmol/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 (10~1 000 μmol/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60 mmol/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a1、a2 和 b 受体拮抗剂联合使用不能消除的NE (1~50 μmol/L)引起的去极化反应。结果提示：NE 可能通过激活一类非a、非b 肾上腺能受体(可能属于g 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。

关键词： 螺旋动脉; 平滑肌细胞; 去甲肾上腺素; 耳蜗

Effects of chloride channel blockers on excitatory junction potentials in smoothmuscle cells of cochlear spiral modiolar artery in guinea pigs

WANG Ying-Zi, LIU Zheng-Jiang, Li Li, Fan Ping, SI Jun-Qiang, Zhao Lei, MA Ke-Tao, ZHU Li, GAO Wei-Jian

Electrophysiological Laboratory, Laboratory of Xinjiang Endemic and Ethnic Diseases, Shihezi University Medical College, Shihezi 832002, China； Department of Physiology, Wuhan University School of Medicine, Wuhan 430071, China； The First Affiliated Hospital of Xinjiang Medical College, Wulumuqi 830054, China

Abstract


Chloride channels have been identified in vascular smooth muscle cells (SMCs). It has been shown that these channels areinvolved in myogenic tone regulation and neuromuscular transmission in various vascular beds. However, whether the chloride channelsare responsible for the formation of excitatory junction potentials (EJPs) of SMCs in the spiral modiolar artery (SMA) remainsunelucidated. 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 recordingtechniques on acutely isolated SMA. It was found that EJP was evoked in the majority of the SMCs (75%, n=49) with an adequateelectronic 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 orDIDS not only inhibited the amplitude but also shortened the duration of EJP. Decrease of extracellular chloride concentration from135.6 mmol/L to 60 mmol/L would enhance EJP. Moreover, IAA-94 (100 μmol/L) and DIDS (200 μmol/L) could reverse the enhancementof EJP 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 membraneof the SMCs, leading to a transmembrane Cl- current. This current is involved, at least partially, in the formation of EJP.

Key words: spiral modiolar artery; smooth muscle cell; norepinephrine; cochlea

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通讯作者：司军强　　E-mail: sijunqiang11@hotmail.com

引用本文：

王英姿, 刘政江, 李丽, 范平, 司军强, 赵磊, 马克涛, 祝丽, 高维建. 氯离子通道阻断剂对豚鼠耳蜗螺旋动脉平滑肌细胞兴奋性接头电位的影响[J]. 生理学报 2006; 58 (5): 456-462.

WANG Ying-Zi, LIU Zheng-Jiang, Li Li, Fan Ping, SI Jun-Qiang, Zhao Lei, MA Ke-Tao, ZHU Li, GAO Wei-Jian. Effects of chloride channel blockers on excitatory junction potentials in smoothmuscle cells of cochlear spiral modiolar artery in guinea pigs. Acta Physiol Sin 2006; 58 (5): 456-462 (in Chinese with English abstract).

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