Protein kinase A-dependent activation of inward rectifier potassium channels by adenosine in rabbit coronary smooth muscle cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Son, Youn Kyoung | - |
dc.contributor.author | Park, Won Sun | - |
dc.contributor.author | Ko, Jae-Hong | - |
dc.contributor.author | Han, Jin | - |
dc.contributor.author | Kim, Nari | - |
dc.contributor.author | Earm, Yung E. | - |
dc.date.accessioned | 2023-06-13T02:42:04Z | - |
dc.date.available | 2023-06-13T02:42:04Z | - |
dc.date.issued | 2005-12 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/66785 | - |
dc.description.abstract | We studied the effect of adenosine on the Ba2+-sensitive K IR channels in the smooth muscle cells isolated from the small-diameter (<100 μm) coronary arteries of rabbit. Adenosine increased KIR currents in concentration-dependent manner (EC50 = 9.4 ± 1.4 μM, maximum increase of 153%). The adenosine-induced stimulation of KIR current was blocked by adenylyl cyclase inhibitor, SQ22536 and was mimicked by adenylyl cyclase activator, forskolin. The adenosine-induced increase of current was blocked by cyclic AMP-dependent protein kinase (PKA) inhibitors, KT 5720 and Rp-8-CPT-cAMPs. The adenosine-induced increase of KIR currents was blocked by an A 3-selective antagonist MRS1334, while the antagonists of other subtypes (DPCPX for A1, ZM241385 for A2A, and alloxazine for A2B) were all ineffective. Furthermore, an A3- selective agonist, 2-Cl-IB-MECA induced increase of KIR currents. We also examined the effect of adenosine on coronary blood flow (CBF) rate by using the Langendorff-perfused heart. In the presence of glibenclamide to exclude the effects of ATP-sensitive K+ (KATP) channels, CBF was increased by adenosine (10 μM), which was blocked by the addition of Ba 2+ (50 μM). Above results suggest that adenosine increases K IR current via A3 subtype through the activation of PKA in rabbit small-diameter coronary arterial smooth muscle cells. © 2005 Elsevier Inc. All rights reserved. | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Academic Press | - |
dc.title | Protein kinase A-dependent activation of inward rectifier potassium channels by adenosine in rabbit coronary smooth muscle cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.bbrc.2005.09.176 | - |
dc.identifier.bibliographicCitation | Biochemical and Biophysical Research Communications, v.337, no.4, pp 1145 - 1152 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000233120600020 | - |
dc.identifier.scopusid | 2-s2.0-27144539171 | - |
dc.citation.endPage | 1152 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 1145 | - |
dc.citation.title | Biochemical and Biophysical Research Communications | - |
dc.citation.volume | 337 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | Adenosine | - |
dc.subject.keywordAuthor | Inward rectifier K+ channel | - |
dc.subject.keywordAuthor | Protein kinase C | - |
dc.subject.keywordAuthor | Coronary artery | - |
dc.subject.keywordPlus | RECEPTOR SUBTYPES | - |
dc.subject.keywordPlus | CEREBRAL-ARTERIES | - |
dc.subject.keywordPlus | RAT | - |
dc.subject.keywordPlus | VASODILATION | - |
dc.subject.keywordPlus | DILATION | - |
dc.subject.keywordPlus | CURRENTS | - |
dc.relation.journalResearchArea | Biochemistry & Molecular BiologyBiophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular BiologyBiophysics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.