highlighted topics Signal Transduction in Smooth Muscle Invited Review: Mechanisms of calcium handling in smooth muscles-猫眼课题宝

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特邀综述：平滑肌肉中钙离子的作用机制。J Appl Physiol 91：1438-1449,2001。-胞浆中钙离子浓度调节平滑肌细胞和组织的收缩状态。细胞内钙离子浓度升高导致细胞收缩是通过细胞内钙离子进入和释放来完成的。钙离子通道包括二氢吡啶敏感和不敏感的钙离子通道和受体非选择性钙离子通道和非选择性钙离子通道。肌浆网(SR)的细胞内释放是通过兰尼定和三磷酸肌醇受体完成的。钙离子进入和释放对胞浆浓度的影响是通过钙离子再摄取到SR、摄取到线粒体和排入细胞外液来调节的。高局域性的钙瞬变(即火花和喷雾)调节质膜上的离子电导，从而对细胞的兴奋性提供反馈，并影响钙离子的进入。这篇简短的综述描述了主要的转运机制和用于在平滑肌肉中处理钙离子的间隔。与肌浆网(SR)和质膜(PM)之间的肌膜下区域、肌浆网(SR)和质膜(PM)之间的肌膜下区域、线粒体(M)和一般细胞质有关。正如文中所讨论的，许多转运蛋白参与了钙离子的调节。去极化激活二氢吡啶敏感的钙通道(DHP Ca21)。其他的钙内流机制包括激动剂激活的非选择性阳离子通道(NSCC，由ﬁGure的毒鼠碱刺激激活)和容量性钙内流(CCE)通道。NSCC中钙离子进入的数量是有争议的，但这些通道产生的去极化激活了DHP的钙离子通道。Ca2 1进入细胞后可增加整体胞浆中的Ca2 1，引起收缩。进入细胞的部分钙离子可能被超ﬁ的钙离子储存所占据(“缓冲”)，如肌质网和线粒体。Sarco(Endo)质网Ca21-ATPase(SERCA)泵提供了将Ca21隔离到SR中的机制，这需要能量将Ca21向上泵入陡峭的浓度梯度。CA 2 1在SR中高度缓冲。线粒体内膜(外膜用虚线示意)中的钙单转运体提供了一种摄取机制，这种摄取发生在电子传输链质子泵产生的大的电化学梯度下。线粒体内的钙平衡是通过钠/钙交换(NCE)来维持的。许多兴奋性激动剂与G蛋白(G_q/G_(11))偶联的受体结合，激活磷脂酶C生成三磷酸肌醇(IP_3)。IP3与SR膜上的受体结合，引起钙释放。这可能与钙2进入机制相结合，并有助于全球性的钙2 1瞬变.IP_3依赖的Ca_2_1也可刺激细胞摄取Ca_2_1

Invited Review: Mechanisms of calcium han- dling in smooth muscles. J Appl Physiol 91: 1438–1449, 2001.—The concentration of cytoplasmic Ca 2 1 regulates the contractile state of smooth muscle cells and tissues. Elevations in global cytoplasmic Ca 2 1 resulting in contraction are accomplished by Ca 2 1 entry and release from intracellular stores. Pathways for Ca 2 1 entry include dihydropyridine-sensitive and -insensitive Ca 2 1 channels and receptor and store-oper-ated nonselective channels permeable to Ca 2 1 . Intracellular release from the sarcoplasmic reticulum (SR) is accomplished by ryanodine and ino- sitol trisphosphate receptors. The impact of Ca 2 1 entry and release on cytoplasmic concentration is modulated by Ca 2 1 reuptake into the SR, uptake into mitochondria, and extrusion into the extracellular solution. Highly localized Ca 2 1 transients (i.e., sparks and puffs) regulate ionic conductances in the plasma membrane, which can provide feedback to cell excitability and affect Ca 2 1 entry. This short review describes the major transport mechanisms and compartments that are utilized for Ca 2 1 handling in smooth muscles. are relevant to Ca 2 1 signaling in smooth muscle: 1 ) extracellular solution, 2 ) subsarcolemmal region between sarcoplasmic reticulum (SR) and plasma membrane (PM), 3 ) SR, 4 ) mitochondria (M), and 5 ) general cytoplasm. As discussed in the text, many transport proteins are involved in Ca 2 1 handling. Depolarization activates dihydropyridine-sensitive Ca 2 1 channels (DHP Ca 2 1 ). Other Ca 2 1 entry mechanisms include agonist-activated nonselective cation channels (NSCC, activated by muscarinic stimulation featured in ﬁgure) and capacitative Ca 2 1 entry (CCE) channels. The amount of Ca 2 1 entry through NSCC is controversial, but these channels yield depolarization that activates DHP Ca 2 1 channels. Ca 2 1 entering cells can increase global cytoplasmic Ca 2 1 and cause contraction. Part of the Ca 2 1 entering cells may be taken up (“buffered”) by superﬁcial Ca 2 1 stores, such as the SR and mitochondria. Sarco(endo)plasmic reticulum Ca 2 1 -ATPase (SERCA) pumps provide the mechanism to sequester Ca 2 1 into the SR, and this requires energy to pump Ca 2 1 up a steep concentration gradient. Ca 2 1 is highly buffered within SR. The Ca 2 1 uniporter in the inner membrane of mitochondria (outer membrane depicted schematically by dotted line) provides an uptake mechanism, and this occurs down a large electrochemical gradient for Ca 2 1 (mitochondria inside very negative) generated by proton pumping by the electron transport chain. Ca 2 1 homeostasis in mitochondria is maintained by Na 1 /Ca 2 1 exchange (NCE). Many excitatory agonists bind to receptors coupled to G proteins (G q /G 11 ) and activate phospho- lipase C to generate inositol trisphosphate (IP 3 ). IP 3 binds to receptors in the SR membrane and causes Ca 2 1 release. This can sum with Ca 2 1 entry mechanisms and contribute to global Ca 2 1 transients. IP 3 -dependent Ca 2 1 can also stimulate Ca 2 1 uptake into

highlighted topics Signal Transduction in Smooth Muscle Invited Review: Mechanisms of calcium handling in smooth muscles

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