Kv7 potassium channels as signal transduction intermediates in the control of microvascular tone Journal Article

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Authors: Byron, K. L.; Brueggemann, L. I.
Article Title: Kv7 potassium channels as signal transduction intermediates in the control of microvascular tone
Abstract: Potassium channels are recognized as important regulators of cellular functions in most, if not all cell types. These cellular proteins assemble to form gated pores in the plasma membrane, which serve to regulate the flow of potassium ions (K(+) ) from the cytosol to the extracellular space. In VSMCs, the open state of potassium channels enables the efflux of K(+) and thereby establishes a negative resting voltage across the plasma membrane that inhibits the opening of VSCCs. Under these conditions, cytosolic Ca(2+) concentrations are relatively low and Ca(2+) -dependent contraction is inhibited. Recent research has identified Kv7 family potassium channels as important contributors to resting membrane voltage in VSMCs, with much of the research focusing on the effects of drugs that specifically activate or block these channels to produce corresponding effects on VSMC contraction and vascular tone. Increasingly, evidence is emerging that these channels are not just good drug targets-they are also essential intermediates in vascular signal transduction, mediating vasoconstrictor or vasodilator responses to a variety of physiological stimuli. This review will summarize recent research findings that support a crucial function of Kv7 channels in both positive (vasoconstrictive) and negative (vasorelaxant) regulation of microvascular tone.
Journal Title: Microcirculation (New York, N.Y.: 1994)
Volume: 25
Issue: 1
ISSN: 1549-8719; 1073-9688
Publisher: Wiley Periodicals, Inc  
Journal Place: United States
Date Published: 2018
Start Page: 10.1111/micc.12419
Language: eng
DOI/URL:

10.1111/micc.12419
Notes: LR: 20180109; CI: (c) 2017; JID: 9434935; OTO: NOTNLM; 2017/07/13 00:00 [received]; 2017/09/27 00:00 [accepted]; 2017/10/05 06:00 [pubmed]; 2017/10/05 06:00 [medline]; 2017/10/05 06:00 [entrez]; ppublish