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Physiological role of inward rectifier K(+) channels in vascular smooth muscle cells

Cited 36 time in Web of Science Cited 37 time in Scopus
Authors
Park, Won Sun; Han, Jin; Earm, Yung E
Issue Date
2008-04-26
Publisher
Springer Verlag
Citation
Pflugers Arch. 457(1):137-147
Keywords
AnimalsArteries/drug effects/physiologyBiological Factors/pharmacologyHumansMyocytes, Smooth Muscle/drug effects/*physiologyNitroprusside/pharmacologyPotassium Channel Blockers/pharmacologyPotassium Channels, Inwardly Rectifying/agonists/antagonists & inhibitors/*physiologyVasoconstrictor Agents/pharmacologyVasodilator Agents/pharmacology
Abstract
K(+) channels play indispensable roles in establishing the membrane potential and in regulating the contractile tone of arterial smooth muscle cells. There are four types of K(+) channels in arterial smooth muscle: voltage-dependent K(+) (K(V)), Ca(2+)-dependent K(+) (BK(Ca)), ATP-dependent K(+) (K(ATP)), and inward rectifier K(+) (Kir2) channels. Comparatively few physiological studies have focused on Kir2 channels because they are present only in certain small-diameter cerebral and submucosal arterioles and in coronary arterial smooth muscle. Here, we review the characteristics and regulation of Kir2 channels in vascular arterial smooth muscle. Current knowledge of the predominant Kir2 channel subtype is Kir2.1, not Kir2.2 and 2.3. Electrophysiological measurements to determine the current-voltage relationship in arterial smooth muscle revealed inward rectification with a single-channel conductance of 21 pS. Kir2 channels were found to influence the resting tone of cerebral and coronary arteries based on the fact that barium (Ba(2+)) induces the constriction of these arteries at resting tone. Kir2 channels are also highly responsive to vasoconstrictors and vasodilators. For example, the vasoconstrictors endothelin-1 and angiotensin II inhibit Kir2 channel function by activating protein kinase C (PKC), and the vasodilator adenosine stimulates Kir2 channel function by increasing the level of cAMP, which subsequently activates protein kinase A (PKA). Certain pathological conditions such as left ventricular hypertrophy are associated with a decrease in Kir2 channel expression. Although our understanding of the physiological role and regulation of Kir2 channels is incomplete, it is believed that Kir2 channels contribute to the control of vascular tone in small-diameter vessels via various intracellular signalling pathways that regulate cell membrane potential.
ISSN
0031-6768 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18437413

http://www.springerlink.com/content/t2w8087qt4586425/fulltext.pdf

http://hdl.handle.net/10371/68173
DOI
https://doi.org/10.1007/s00424-008-0512-7
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Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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