Activation of inward rectifier K+ channels by hypoxia in rabbit coronary arterial smooth muscle cells
DC Field | Value | Language |
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dc.contributor.author | Park, Won Sun | - |
dc.contributor.author | Han, Jin | - |
dc.contributor.author | Kim, Nari | - |
dc.contributor.author | Ko, Jae-Hong | - |
dc.contributor.author | Kim, Sung Joon | - |
dc.contributor.author | Earm, Yung E | - |
dc.date.accessioned | 2023-06-13T02:41:59Z | - |
dc.date.available | 2023-06-13T02:41:59Z | - |
dc.date.issued | 2005-12 | - |
dc.identifier.issn | 0363-6135 | - |
dc.identifier.issn | 1522-1539 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/66784 | - |
dc.description.abstract | We examined the effects of acute hypoxia on Ba2+-sensitive inward rectifier K+ (KIR) current in rabbit coronary arterial smooth muscle cells. The amplitudes of KIR current was definitely higher in the cells from small-diameter (<100 μm) coronary arterial smooth muscle cells (SCASMC, -12.8 ± 1.3 pA/pF at -140 mV) than those in large-diameter coronary arterial smooth muscle cells (>200 μm, LCASMC, -1.5 ± 0.1 pA pF-1). Western blot analysis confirmed that Kir2.1 protein was expressed in SCASMC but not LCASMC. Hypoxia activated much more KIR currents in symmetrical 140 K+. This effect was blocked by the adenylyl cyclase inhibitor SQ-22536 (10 μM) and mimicked by forskolin (10 μM) and dibutyryl-cAMP (500 μM). The production of cAMP in SCASMC increased 5.7-fold after 6 min of hypoxia. Hypoxia-induced increase in KIR currents was abolished by the PKA inhibitors, Rp-8-(4-chlorophenylthio)-cAMPs (10 μM) and KT-5720 (1 μM). The inhibition of G protein with GDPβS (1 mM) partially reduced (∼50%) the hypoxia-induced increase in KIR currents. In Langendorff-perfused rabbit hearts, hypoxia increased coronary blood flow, an effect that was inhibited by Ba2+. In summary, hypoxia augments the KIR currents in SCASMC via cAMP- and PKA-dependent signaling cascades, which might, at least partly, explain the hypoxia-induced coronary vasodilation. Copyright © 2005 the American Physiological Society. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | American Physiological Society | - |
dc.title | Activation of inward rectifier K+ channels by hypoxia in rabbit coronary arterial smooth muscle cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.1152/ajpheart.00331.2005 | - |
dc.identifier.bibliographicCitation | American Journal of Physiology - Heart and Circulatory Physiology, v.289, no.6, pp H2461 - H2467 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000233176600026 | - |
dc.identifier.scopusid | 2-s2.0-27144549180 | - |
dc.citation.endPage | H2467 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | H2461 | - |
dc.citation.title | American Journal of Physiology - Heart and Circulatory Physiology | - |
dc.citation.volume | 289 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | inwardly rectifying K+ currentcoronary vasodilationprotein kinase AKir2.1 | - |
dc.subject.keywordPlus | SENSITIVE POTASSIUM CHANNELS | - |
dc.subject.keywordPlus | MIDDLE CEREBRAL-ARTERIES | - |
dc.subject.keywordPlus | EXTRACELLULAR POTASSIUM | - |
dc.subject.keywordPlus | BLOOD-FLOW | - |
dc.subject.keywordPlus | RAT CORONARY | - |
dc.subject.keywordPlus | ATP-CHANNELS | - |
dc.subject.keywordPlus | ENDOTHELIUM | - |
dc.subject.keywordPlus | ADENOSINE | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | GLIBENCLAMIDE | - |
dc.relation.journalResearchArea | Cardiovascular System & CardiologyPhysiology | - |
dc.relation.journalWebOfScienceCategory | Cardiac & Cardiovascular SystemsPhysiologyPeripheral Vascular Disease | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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