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首页> 外文期刊>American Journal of Physiology >Calcium waves in intact guinea pig gallbladder smooth muscle cells.
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Calcium waves in intact guinea pig gallbladder smooth muscle cells.

机译：完整豚鼠胆囊平滑肌细胞中的钙波。

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摘要

Intracellular Ca(2+) waves and spontaneous transient depolarizations were investigated in gallbladder smooth muscle (GBSM) whole mount preparations with intact mucosal layer [full thickness (FT)] by laser confocal imaging of intracellular Ca(2+) and voltage recordings with microelectrodes, respectively. Spontaneous Ca(2+) waves arose most often near the center, but sometimes from the extremities, of GBSM cells. They propagated regeneratively by Ca(2+)-induced Ca(2+) release involving inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)] receptors and were not affected by TTX and atropine (ATS). Spontaneous Ca(2+) waves and spontaneous transient depolarizations were more prevalent in FT than in isolated muscularis layer preparations and occurred with similar pattern in GBSM bundles. Ca(2+) waves were abolished by the Ins(1,4,5)P(3) receptor inhibitors 2-aminoethoxydiphenyl borate and xestospongin C and by caffeine and cyclopiazonic acid. These events were reduced by voltage-dependent calcium channels (VDCCs) inhibitors diltiazem and nifedipine, by PLC inhibitor U-73122, and by thapsigargin and ryanodine. ACh, CCK, and carbachol augmented Ca(2+) waves and induced Ca(2+) flashes. The actions of these agonists were inhibited by U-73122. These results indicate that in GBSM, discharge and propagation of Ca(2+) waves depend on sarco(endo)plasmic reticulum (SR) Ca(2+) release via Ins(1,4,5)P(3) receptors, PLC activity, Ca(2+) influx via VDCCs, and SR Ca(2+) concentration. Neurohormonal enhancement of GBSM excitability involves PLC-dependent augmentation and synchronization of SR Ca(2+) release via Ins(1,4,5)P(3) receptors. Ca(2+) waves likely reflect the activity of a fundamental unit of spontaneous activity and play an important role in the excitability of GBSM.
机译：通过细胞内Ca（2+）的激光共聚焦成像和微电极电压记录，研究了具有完整粘膜层[全厚度（FT）]的胆囊平滑肌（GBSM）整装制剂中的细胞内Ca（2+）波和自发性瞬时去极化， 分别。自发的Ca（2+）波最常出现在GBSM细胞的中心附近，但有时从四肢开始。它们通过涉及肌醇1,4,5-三磷酸[Ins（1,4,5）P（3）]受体的Ca（2+）诱导的Ca（2+）释放而再生繁殖，并且不受TTX和阿托品（ ATS）。自发的Ca（2+）波和自发的瞬时去极化在FT中比在孤立的肌层制备中更普遍，并且在GBSM束中以相似的模式发生。 Ca（2+）波被Ins（1,4,5）P（3）受体抑制剂2-氨基乙氧基二苯基硼酸酯和异黄酮C以及咖啡因和环吡嗪酸消除。这些事件通过电压依赖性钙通道（VDCCs）抑制剂地尔硫卓和硝苯地平，PLC抑制剂U-73122以及毒胡萝卜素和ryanodine减少。 ACh，CCK和卡巴胆碱增加Ca（2+）波和诱导Ca（2+）闪烁。这些激动剂的作用被U-73122抑制。这些结果表明，在GBSM中，Ca（2+）波的放电和传播取决于肌（内）质网（SR）Ca（2+）通过Ins（1,4,5）P（3）受体，PLC释放活动，Ca（2+）通过VDCC流入和SR Ca（2+）浓度。 GBSM兴奋性的神经激素增强涉及通过Ins（1,4,5）P（3）受体的PLC依赖性增强和SR Ca（2+）释放的同步。 Ca（2+）波可能反映自发活动的基本单位的活动，并在GBSM的兴奋性中起重要作用。

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