Journal ArticleDOI
K+ channel modulation in arterial smooth muscle
N B Standen,J M Quayle +1 more
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TLDR
Arterial K+ channels are modulated by physiological vasodilators, which increase K+ channel activity, and vasoconstrictors, which decrease it, which makes important contributions to the regulation of blood flow.Abstract:
Potassium channels play an essential role in the membrane potential of arterial smooth muscle, and also in regulating contractile tone. Four types of K+ channel have been described in vascular smooth muscle: Voltage-activated K+ channels (Kv) are encoded by the Kv gene family, Ca(2+)-activated K+ channels (BKCa) are encoded by the slo gene, inward rectifiers (KIR) by Kir2.0, and ATP-sensitive K+ channels (KATP) by Kir6.0 and sulphonylurea receptor genes. In smooth muscle, the channel subunit genes reported to be expressed are: Kv1.0, Kv1.2, Kv1.4-1.6, Kv2.1, Kv9.3, Kv beta 1-beta 4, slo alpha and beta, Kir2.1, Kir6.2, and SUR1 and SUR2. Arterial K+ channels are modulated by physiological vasodilators, which increase K+ channel activity, and vasoconstrictors, which decrease it. Several vasodilators acting at receptors linked to cAMP-dependent protein kinase activate KATP channels. These include adenosine, calcitonin gene-related peptide, and beta-adrenoceptor agonists. beta-adrenoceptors can also activate BKCa and Kv channels. Several vasoconstrictors that activate protein kinase C inhibit KATP channels, and inhibition of BKCa and Kv channels through PKC has also been described. Activators of cGMP-dependent protein kinase, in particular NO, activate BKCa channels, and possibly KATP channels. Hypoxia leads to activation of KATP channels, and activation of BKCa channels has also been reported. Hypoxic pulmonary vasoconstriction involves inhibition of Kv channels. Vasodilation to increased external K+ involves KIR channels. Endothelium-derived hyperpolarizing factor activates K+ channels that are not yet clearly defined. Such K+ channel modulations, through their effects on membrane potential and contractile tone, make important contributions to the regulation of blood flow.read more
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Physiological roles of K^+ channels in vascular smooth muscle cells(Hirosi Kuriyama Award 2007 Memorial Review)
TL;DR: In this paper, the basic properties, physiological functions, regulation, and pathological alterations of four major classes of K+ channels that have been detected in vascular smooth muscle cells are presented, including voltage-dependent K+ (Kv) channels, which open upon depolarization of the plasma membrane.
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References
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Journal ArticleDOI
Physiological roles and properties of potassium channels in arterial smooth muscle
Mark T. Nelson,J. M. Quayle +1 more
TL;DR: The main conclusions of this review are: 1) regulation of arterial smooth muscle membrane potential through activation or inhibition of K+ channel activity provides an important mechanism to dilate or constrict arteries; 2) KV, KCa, KIR, and KATP channels serve unique functions in the regulation of artery membrane potential
Journal ArticleDOI
Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle
TL;DR: Evidence is presented that both exogenous nitric oxide and native EDRF can directly activate single Ca2+-dependent K+ channels (K+Ca) in cell-free membrane patches without requiring cGMP.
Journal ArticleDOI
Calcium channels, potassium channels, and voltage dependence of arterial smooth muscle tone
TL;DR: It is shown that voltage-dependent Ca channels in the steady state can be open and very sensitive to membrane potential changes in a range that occurs in resistance arteries with tone.
Journal ArticleDOI
Primary structure and functional expression of a mouse inward rectifier potassium channel
TL;DR: The IRK1 channel and an ATP-regulated K+ channel show extensive sequence similarity and constitute a new superfamily, similar to the inner core structure of voltage-gated K+ channels.
Journal ArticleDOI
ATP-sensitive and inwardly rectifying potassium channels in smooth muscle
TL;DR: Together, KATP and KIR channels are important regulators of smooth muscle function and represent important therapeutic targets.
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