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KATP channel action in vascular tone regulation: from genetics to diseases

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Author:: No author available

Journal Title:: Acta Physiologica Sinica

Issue:: 1

DOI:: No doi available

Key Word:: ATP敏感钾通道;内向整流钾离子通道亚基6.1;磺脲受体调节亚基2B;蛋白磷酸化;核因子-κB;脓毒血症;婴儿猝死综合征;J波综合征;ATP-sensitive potassium channel;Kir6.1;SUR2B;protein phosphorylation;S-glutathionylation;nuclear factor-κB;sepsis;sudden infant death syndrome;J-wave syndrome

Abstract： ATP-sensitive potassium (KATP) channels are widely distributed in vasculatures,and play an important role in the vascular tone regulation.The KATP channels consist of 4 pore-forming inward rectifier K+ channel (Kir) subunits and 4 regulatory sulfonylurea receptors (SUR).The major vascular isoform of KATP channels is composed of Kir6.1/SUR2B,although low levels of other subunits are also present in vascular beds.The observation from transgenic mice and humans carrying Kir6.1/SUR2B channel mutations strongly supports that normal activity of the Kir6.1/SUR2B channel is critical for cardiovascular function.The Kir6.1/SUR2B channel is regulated by intracellular ATP and ADP.The channel is a common target of several vasodilators and vasoconstrictors.Endogenous vasopressors such as arginine vasopressin and a-adrenoceptor agonists stimulate protein kinase C (PKC) and inhibit the KATP channels,while vasodilators such as β-adrenoceptor agonists and vasoactive intestinal polypeptide increase KATP channel activity by activating the adenylate cyclase-cAMP-protein kinase A (PKA) pathway.PKC phosphorylates a cluster of 4 serine residues at C-terminus of Kir6.1,whereas PKA acts on Serl 387 in the nucleotide binding domain 2 of SUR2B.The Kir6.1/SUR2B channel is also inhibited by oxidants including reactive oxygen species allowing vascular regulation in oxidative stress.The molecular basis underlying such a channel inhibition is likely to be mediated by S-glutathionylation at a few cysteine residues,especially Cys176,in Kir6.1.Furthermore,the channel activity is augmented in endotoxemia or septic shock,as a result of the upregulation of Kir6.1/SUR2B expression.Activation of the nuclear factor-κB dependent transcriptional mechanism contributes to the Kir6.1/SUR2B channel upregulation by lipopolysaccharides and perhaps other toll-like receptor ligands as well.In this review,we summarize the vascular KATP channel regulation under physiological and pathophysiological conditions,and discuss the importance of KATP channel as a potentially useful target in the treatment and prevention of cardiovascular diseases.

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