Synchrony of spontaneous Ca2+ activity in microvascular mural cells.

Q3 Medicine
Retsu Mitsui, Hikaru Hashitani
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引用次数: 5

Abstract

Spontaneous rhythmic constrictions known as vasomotion are developed in several microvascular beds in vivo. Vasomotion in arterioles is considered to facilitate blood flow, while venular vasomotion would facilitate tissue metabolite drainage. Mechanisms underlying vasomotion periodically generate synchronous Ca2+ transients in vascular smooth muscle cells (VSMCs). In visceral organs, mural cells (pericytes and VSMCs) in arterioles, capillaries and venules exhibit synchronous spontaneous Ca2+ transients. Since sympathetic regulation is rather limited in the intra-organ microvessels, spontaneous activity of mural cells may play an essential role in maintaining tissue perfusion. Synchronous spontaneous Ca2+ transients in precapillary arterioles (PCAs)/capillaries appear to propagate to upstream arterioles to drive their vasomotion, while venules develop their own synchronous Ca2+ transients and associated vasomotion. Spontaneous Ca2+ transients of mural cells primarily arise from IP3 and/or ryanodine receptor-mediated Ca2+ release from sarcoendoplasmic reticulum (SR/ER) Ca2+ stores. The resultant opening of Ca2+-activated Cl- channels (CaCCs) causes a membrane depolarisation that triggers Ca2+ influx via T-type and/or L-type voltage-dependent Ca2+ channels (VDCCs). Mural cells are electrically coupled with each other via gap junctions, and thus allow the sequential spread of CaCC or VDCC-dependent depolarisations to develop the synchrony of Ca2+ transients within their network. Importantly, the synchrony of spontaneous Ca2+ transients also requires a certain range of the resting membrane potential that is maintained by the opening of Kv7 voltage-dependent K+ (Kv7) and inward rectifier K+ (Kir) channels. Thus, a depolarised membrane would evoke asynchronous, 'premature' spontaneous Ca2+ transients, while a hyperpolarised membrane prevents any spontaneous activity.

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Abstract Image

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微血管壁细胞自发Ca2+活性的同步性。
自发性节律性收缩称为血管舒缩在体内的几个微血管床中发展。小动脉的血管舒缩被认为可以促进血液流动,而静脉血管舒缩可以促进组织代谢物的排出。血管运动的机制周期性地在血管平滑肌细胞(VSMCs)中产生同步Ca2+瞬态。在内脏器官中,小动脉、毛细血管和小静脉中的壁细胞(周细胞和VSMCs)表现出同步的自发Ca2+瞬态。由于交感调节在器官内微血管中相当有限,壁细胞的自发活动可能在维持组织灌注中起重要作用。在毛细管前小动脉(pca)/毛细血管中同步自发Ca2+瞬变似乎传播到上游小动脉以驱动其血管运动,而小静脉则发展自己的同步Ca2+瞬变和相关的血管运动。壁细胞的自发Ca2+瞬态主要由IP3和/或ryanodine受体介导的肌内质网(SR/ER) Ca2+储存的Ca2+释放引起。由此产生的Ca2+激活的Cl-通道(CaCCs)的开放导致膜去极化,通过t型和/或l型电压依赖性Ca2+通道(VDCCs)触发Ca2+内流。壁细胞通过间隙连接相互电偶联,从而允许CaCC或vdcc依赖的去极化的顺序扩散,以在其网络内发展Ca2+瞬态的同步性。重要的是,自发Ca2+瞬态的同步还需要一定范围的静息膜电位,这是通过打开Kv7电压依赖性K+ (Kv7)和内向整流K+ (Kir)通道来维持的。因此,去极化膜会引起异步的、“过早的”自发Ca2+瞬态,而超极化膜则会阻止任何自发活动。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Smooth Muscle Research
Journal of Smooth Muscle Research Biochemistry, Genetics and Molecular Biology-Physiology
CiteScore
2.30
自引率
0.00%
发文量
7
审稿时长
10 weeks
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