Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.
Calcium-Dependent Ion Channels and the Regulation of Arteriolar Myogenic Tone.
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钙依赖性离子通道和小动脉肌原张力的调节。
DOI：
10.3389/fphys.2021.770450
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发表时间：
2021
影响因子：
4
通讯作者：
Jackson WF
中科院分区：
文献类型：
--
作者：
Jackson WF
外周微循环中的微动脉调节组织和器官内的血液流动，控制毛细血管血压和微血管液体交换，调节外周血管阻力，并有助于调节血压。这些重要的微血管显示压力依赖的肌张力，血管平滑肌细胞(VSMCs)收缩活动的稳定水平，设定静止的小动脉内径，使小动脉既可以扩张，也可以收缩，以满足其灌流的组织和器官的血流和压力需求。这一观点将集中在微动脉VSMCs和调节微动脉张力的内皮细胞(ECs)的血浆和内质网膜上的钙离子依赖的离子通道。在VSMC中，钙依赖的肌张力负反馈调节是由钙激活的钾通道(BKCa)和电压门控钙通道(VGCC)介导的。瞬时受体电位亚家族M，成员4通道(TRPM4)；钙激活的ClATP通道(CaCCs；TMEM16A/ANO1)；钙依赖抑制电压门控性K+(KV)和−敏感性K+(KATP)通道；以及钙通过三磷酸肌醇受体(IP3R)诱导的钙释放参与钙依赖的肌源性张力正反馈调节。VSMC ryanodine受体(RyRs)的钙释放通过钙离子火花介导的BKCa通道活性的调节或与IP3Rs或CaCCs协同的正反馈调节来提供负反馈。在一些小动脉中，VSMC RyR是无声的。在内皮细胞中，瞬时受体电位香草素家族成员4(TRPV4)通道产生激活IP3R的小片钙离子通道和引起膜超极化的中小电导钙激活钾通道(IKCa和sKCa)，膜超极化被传导到覆盖的VSMCs，产生内皮依赖性超极化和血管扩张。内皮细胞IP3R产生钙脉冲星、钙波、钙波和升高的全局钙离子水平，激活EC sKCa和IKCa通道，引起内皮血管扩张剂类物质如NO、前列腺素I2和花生四烯酸环氧化物的钙依赖性产生，介导肌源性张力的负反馈调节。因此，钙离子依赖的离子通道在微循环中对微动脉肌张力调节的许多方面起着重要作用。
Arterioles in the peripheral microcirculation regulate blood flow to and within tissues and organs, control capillary blood pressure and microvascular fluid exchange, govern peripheral vascular resistance, and contribute to the regulation of blood pressure. These important microvessels display pressure-dependent myogenic tone, the steady state level of contractile activity of vascular smooth muscle cells (VSMCs) that sets resting arteriolar internal diameter such that arterioles can both dilate and constrict to meet the blood flow and pressure needs of the tissues and organs that they perfuse. This perspective will focus on the Ca2+-dependent ion channels in the plasma and endoplasmic reticulum membranes of arteriolar VSMCs and endothelial cells (ECs) that regulate arteriolar tone. In VSMCs, Ca2+-dependent negative feedback regulation of myogenic tone is mediated by Ca2+-activated K+ (BKCa) channels and also Ca2+-dependent inactivation of voltage-gated Ca2+ channels (VGCC). Transient receptor potential subfamily M, member 4 channels (TRPM4); Ca2+-activated Cl− channels (CaCCs; TMEM16A/ANO1), Ca2+-dependent inhibition of voltage-gated K+ (KV) and ATP-sensitive K+ (KATP) channels; and Ca2+-induced-Ca2+ release through inositol 1,4,5-trisphosphate receptors (IP3Rs) participate in Ca2+-dependent positive-feedback regulation of myogenic tone. Calcium release from VSMC ryanodine receptors (RyRs) provide negative-feedback through Ca2+-spark-mediated control of BKCa channel activity, or positive-feedback regulation in cooperation with IP3Rs or CaCCs. In some arterioles, VSMC RyRs are silent. In ECs, transient receptor potential vanilloid subfamily, member 4 (TRPV4) channels produce Ca2+ sparklets that activate IP3Rs and intermediate and small conductance Ca2+ activated K+ (IKCa and sKCa) channels causing membrane hyperpolarization that is conducted to overlying VSMCs producing endothelium-dependent hyperpolarization and vasodilation. Endothelial IP3Rs produce Ca2+ pulsars, Ca2+ wavelets, Ca2+ waves and increased global Ca2+ levels activating EC sKCa and IKCa channels and causing Ca2+-dependent production of endothelial vasodilator autacoids such as NO, prostaglandin I2 and epoxides of arachidonic acid that mediate negative-feedback regulation of myogenic tone. Thus, Ca2+-dependent ion channels importantly contribute to many aspects of the regulation of myogenic tone in arterioles in the microcirculation.
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影响因子：
20.1
作者：
Borisova, Lyudmyla;Wray, Susan;Burdyga, Theodor
通讯作者：
Burdyga, Theodor
影响因子：
4.4
作者：
Curtis TM;Tumelty J;Dawicki J;Scholfield CN;McGeown JG
通讯作者：
McGeown JG
影响因子：
4.5
作者：
Bulley, Simon;Jaggar, Jonathan H.
通讯作者：
Jaggar, Jonathan H.
影响因子：
15.9
作者：
Amberg, GC;Bonev, AD;Santana, LF
通讯作者：
Santana, LF
影响因子：
20.1
作者：
Cartin, L;Lounsbury, KM;Nelson, MT
通讯作者：
Nelson, MT