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Multiple regulatory effects of angiotensin II on the large-conductance Ca2+- and voltage-activated potassium channel in vascular smooth muscle cells

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Author:: No author available

Journal Title:: Acta Physiologica Sinica

Issue:: 2

DOI:: 10.13294/j.aps.2019.0013

Key Word:: 大电导钙激活钾通道;血管紧张素II;血管紧张素II-1型受体;血管平滑肌;large-conductance Ca2+- and voltage-activated potassium channel;angiotensin II;angiotensin II type 1 receptor;vascular smooth muscle

Abstract： Renin-angiotensin system(RAS) is involved in the regulation of vascular smooth muscle cell(VSMC) tension.Angiotensin II(Ang II) as the main effector molecule of RAS can increase the intracellular Ca2+ concentration and cause VSMCs contraction by activating angiotensin II type 1 receptor(AT1R).The large-conductance Ca2+- and voltage-activated potassium(BK) channel is an essen-tial potassium channel in VSMCs,playing an important role in maintaining membrane potential and intracellular potassium-calcium balance.The BK channel in VSMCs mainly consists of α and β1 subunits.Functional BKα subunits contain voltage-sensors and Ca2+ binding sites.Hence,increase in the membrane potential or intracellular Ca2+ concentration can trigger the opening of the BK channel by mediating transient K+ outward current in a negative regulatory manner.However,increasing evidence has shown that although Ang II can raise the intracellular Ca2+ concentration,it also inhibits the expression and function of the BK channel by activating the PKC pathway,internalizing AT1R-BKα heterodimer,or dissociating α and β1 subunits.Under some specific conditions,Ang II can also activate the BK channel,but the underlying mechanism remains unknown.In this review,we summarize the potential mecha-nisms underlying the inhibitory or activating effect of Ang II on the BK channel,hoping that it could provide a theoretical basis for improving intracellular ion imbalance.

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