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首页> 外文期刊>Life sciences >Capacitative calcium entry in guinea pig gallbladder smooth muscle in vitro
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Capacitative calcium entry in guinea pig gallbladder smooth muscle in vitro

机译：豚鼠胆囊平滑肌中钙离子的体外吸收

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This study investigates the involvement of capacitative Ca2+ entry in excitation-contraction coupling in guinea pig gallbladder smooth muscle. Thapsigargin (0.1 nM- I muM, a sarcoplasmic reticulum Ca2+-ATPase inhibitor) produced slowly developing sustained tonic contractions in guinea pig isolated gallbladder strips. All contractions approached 50% of the response to carbachol (10 muM) after 55 min. Contractile responses to thapsigargin (1 muM) were abolished in a Ca2+-free medium. Subsequent re-addition of Ca2+ (2.5 mM) produced a sustained tonic contraction (99 +/- 6% of the carbachol response). The contractile response to Ca2+ re-addition following incubation of tissues in a Ca2+-free bathing solution in the absence of thapsigargin was significantly less than in its presence (79 +/- 4 % vs 100 +/- 7 % of carbachol; p < 0.05). Contractile responses to Ca2+ re-addition following treatment with thapsigargin were attenuated by (a) the L-type voltage-operated Ca2+ channel antagonist, nifedipine (10 muM) and (b) the general inhibitor of Ca2+ entry channels including store-operated channels, SKF96365 (50 muM and 100 muM). In separate experiments, responses to Ca2+ re-addition were essentially abolished by the tyrosine kinase inhibitor, genistein (100 muM). These results suggest that capacitative Ca2+ entry provides a source of activator Ca2+ for guinea pig gallbladder smooth muscle contraction. Contractile responses to Ca2+ re-addition following depletion of sarcoplasmic reticulum Ca2+ stores with thapsigargin, are mediated in part by Ca2+ entry through voltage-operated Ca2+ channels and by capacitative Ca2+ entry through store-operated Ca2+ channels which can be blocked by SK&F96365. Furthermore, capacitative Ca2+ entry in this tissue may be modulated by tyrosine kinase. (C) 2003 Elsevier Inc. All rights reserved. [References: 37]
机译：这项研究调查了电容性Ca2 +进入在豚鼠胆囊平滑肌兴奋收缩耦合中的作用。 Thapsigargin（0.1 nM-1μM，肌浆网Ca2 + -ATPase抑制剂）在豚鼠分离的胆囊条中缓慢产生持续的强直性收缩。 55分钟后，所有收缩均达到对卡巴胆碱（10μM）反应的50％。在无Ca2 +的培养基中消除了对毒胡萝卜素（1 muM）的收缩反应。随后重新添加Ca2 +（2.5 mM）产生了持续的强直收缩（99％+/- 6％的卡巴胆碱反应）。在无毒胡萝卜素的情况下在不含Ca2 +的沐浴溶液中组织培养后，对Ca2 +重新添加的收缩反应显着小于其存在时的收缩反应（79 +/- 4％对100 +/- 7％的卡巴胆碱; p < 0.05）。 thapsigargin处理后，对Ca2 +重新添加的收缩反应被（a）L型电压操纵的Ca2 +通道拮抗剂，硝苯地平（10μM）和（b）Ca2 +进入通道的一般抑制剂（包括贮存操作通道）减弱了， SKF96365（50μM和100μM）。在单独的实验中，酪氨酸激酶抑制剂染料木黄酮（100μM）基本上消除了对Ca2 +重新添加的反应。这些结果表明，电容性Ca2 +进入为豚鼠胆囊平滑肌收缩提供了激活剂Ca2 +。肉碱质网中的thapsigargin耗尽了肌钙蛋白Ca2 +存储后，对Ca2 +重新添加的收缩反应部分由通过电压操作的Ca2 +通道进入的Ca2 +进入以及通过可被SK＆F96365阻止的通过存储操作的Ca2 +通道进入的电容性Ca2 +介导。此外，酪氨酸激酶可调节该组织中的电容性Ca2 +进入。 （C）2003 Elsevier Inc.保留所有权利。 [参考：37]

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