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KATP Channels in Vascular Smooth Muscle: Structure, Regulation and Functional Roles

Journal of Clinical and Basic Cardiology 2003; 6 (1-4): 7-14

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Fig. 1: KTP-Kanal - Regulation

Keywords: BlutflussGlatte MuskelzelleKardiologieKATP-KanalVasodilatationVasokonstriktionblood flowcardiologyKATP-channelsmooth muscle cellvasoconstrictionVasodilatation

KATP channels link membrane K+ permeability to metabolism. In vascular smooth muscle, the molecular composition of the channel isoforms expressed has not been determined definitively, though there is good evidence that a channel comprising the pore-forming subunit Kir6.1 and the sulphonylurea receptor SUR2B plays important roles. It is also likely that there is molecular diversity among KATP channels of smooth muscle, with the possible involvement of heterotetramers of pore-forming subunits. In addition to metabolic regulation, vascular KATP channels are regulated by endogenous vasoactive agents by way of cellular signalling pathways. Protein kinase A has been shown both to cause tonic channel activation, and to be important in activation by several vasodilators. These actions require PKA localization by an A-kinase anchoring protein (AKAP). Vasoconstrictors cause channel inhibition by way of protein kinase C, and vascular KATP channels have also been shown to be inhibited by intracellular calcium, an effect mediated by protein phosphatase 2B. Physiologically, KATP channels appear to be involved in the maintenance of resting blood flow in a number of vascular beds, notably the coronary circulation, as well as in vasodilation in response to metabolic demand. There is also increasing evidence for a pathophysiological role in the catastrophic vasodilation and vascular hyporeactivity of circulatory shock. Clinically, the KATP opener nicorandil is increasingly used in angina, where it may show maximum potency in ischaemic tissue, while increased understanding of these channels may offer future therapeutic opportunities.
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