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首页> 外文期刊>American Journal of Physiology >Spontaneous electrical rhythmicity and the role of the sarcoplasmic reticulum in the excitability of guinea pig gallbladder smooth muscle cells.
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Spontaneous electrical rhythmicity and the role of the sarcoplasmic reticulum in the excitability of guinea pig gallbladder smooth muscle cells.

机译：自发性电节律和肌浆网在豚鼠胆囊平滑肌细胞兴奋性中的作用。

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摘要

Spontaneous action potentials and Ca(2+) transients were investigated in intact gallbladder preparations to determine how electrical events propagate and the cellular mechanisms that modulate these events. Rhythmic phasic contractions were preceded by Ca(2+) flashes that were either focal (limited to one or a few bundles), multifocal (occurring asynchronously in several bundles), or global (simultaneous flashes throughout the field). Ca(2+) flashes and action potentials were abolished by inhibiting sarcoplasmic reticulum (SR) Ca(2+) release via inositol (1,4,5)-trisphosphate [Ins(1,4,5)P(3)] channels with 2-aminoethoxydiphenyl borate and xestospongin C or by inhibiting voltage-dependent Ca(2+) channels (VDCCs) with nifedipine or diltiazem or nisoldipine. Inhibiting ryanodine channels with ryanodine caused multiple spikes superimposed upon plateaus of action potentials and extended quiescent periods. Depletion of SR Ca(2+) stores with thapsigargin or cyclopiazonic acid increased the frequency and duration of Ca(2+) flashes and action potentials. Acetylcholine, carbachol, or cholecystokinin increased synchronized and increased the frequency of Ca(2+) flashes and action potentials. The phospholipase C (PLC) inhibitor U-73122 did not affect Ca(2+) flash or action potential activity but inhibited the excitatory effects of acetylcholine on these events. These results indicate that Ca(2+) flashes correspond to action potentials and that rhythmic excitation in the gallbladder is multifocal among gallbladder smooth muscle bundles and can be synchronized by excitatory agonists. These events do not depend on PLC activation, but agonist stimulation involves activation of PLC. Generation of these events depends on Ca(2+) entry via VDCCs and on Ca(2+) mobilization from the SR via Ins(1,4,5)P(3) channels.
机译：在完整的胆囊准备中研究自发性动作电位和Ca（2+）瞬变，以确定电事件如何传播以及调节这些事件的细胞机制。在有节奏的相收缩之前，出现Ca（2+）闪烁，这些闪烁是焦点性的（限于一束或几束），多焦点的（在几束中异步发生）或全局性的（整个场中同时闪烁）。 Ca（2+）闪烁和动作电位通过抑制肌质网（SR）通过肌醇（1,4,5）-三磷酸[Ins（1,4,5）P（3）]通道释放Ca（2+）用2-氨基乙氧基二苯基硼酸酯和xestospongin C或通过用硝苯地平或地尔硫卓或尼索地平抑制电压依赖性Ca（2+）通道（VDCC）。用ryanodine抑制ryanodine通道会导致多个尖峰叠加在动作电位的平台上，并延长了静止期。与thapsigargin或Cyclpiazonic酸的SR Ca（2+）存储的耗尽增加了Ca（2+）闪烁和动作电位的频率和持续时间。乙酰胆碱，卡巴胆碱或胆囊收缩素增加同步，并增加Ca（2+）闪烁和动作电位的频率。磷脂酶C（PLC）抑制剂U-73122不会影响Ca（2+）闪光或动作电位活性，但会抑制乙酰胆碱对这些事件的兴奋作用。这些结果表明，Ca（2+）闪烁对应于动作电位，并且胆囊中的节奏性兴奋在胆囊平滑肌束之间是多焦点的，并且可以通过兴奋性激动剂来同步。这些事件不依赖于PLC的激活，但激动剂刺激涉及PLC的激活。这些事件的生成取决于通过VDCCs进入Ca（2+），并取决于通过Ins（1,4,5）P（3）通道从SR迁移Ca（2+）。

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