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
Received: Accepted:
Corresponding author: 司军强 E-mail: sijunqiang11@hotmail.com
Citing This Article：
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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