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• W1981889097 abstract "Voltage-gated, delayed rectifier K + current (K V ) that is sensitive to 4-aminopyridine (4AP) block has been identified in all vascular smooth muscle tissues studied to date. These channels conduct outward, hyperpolarizing K + current that influences resting membrane potential and contributes to repolarization of action potentials. Smooth muscle cells in most arterial resistance vessels regulate Ca 2+ influx and contractile tone by low amplitude, tonic changes in membrane potential. Block of K V with 4-aminopyridine leads to contraction and an enhanced myogenic response to increased intravascular pressure. We investigated the modulation of K V currents in isolated, freshly dispersed smooth muscle cells from rabbit portal vein and coronary arteries in whole-cell voltage clamp experiments. Our findings indicate that K V channels are regulated by signal transduction mechanisms involving vasoactive agonists that activate cAMP-dependent protein kinase (PKA) or protein kinase C (PKC). In this paper, the properties and potential function of K V channels in vascular smooth muscle are reviewed. Further, the regulation and potential role of alterations in K V due to β-adrenoceptor agonists, adenylyl cyclase and PKA, as well as angiotensin II, diacylglycerol, and PKC are discussed.Key words: potassium channels, smooth muscle, protein kinase A, protein kinase C, membrane potential." @default.
• W1981889097 created "2016-06-24" @default.
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• W1981889097 date "1996-07-01" @default.
• W1981889097 modified "2023-09-26" @default.
• W1981889097 title "Regulation of 4-aminopyridine-sensitive, delayed rectifier K⁺ channels in vascular smooth muscle by phosphorylation" @default.
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• W1981889097 doi "https://doi.org/10.1139/o96-048" @default.
• W1981889097 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8960350" @default.
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