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Mechanosensitive nonselective cation channel facilitation by endothelin-1 is regulated by protein kinase C in arterial myocytes

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dc.contributor.authorLee, Hyang Ae-
dc.contributor.authorBaek, Eun Bok-
dc.contributor.authorPark, Kyung Sun-
dc.contributor.authorJung, Hoi Jong-
dc.contributor.authorKim, Jae Il-
dc.contributor.authorKim, Sung Joon-
dc.contributor.authorEarm, Yung E-
dc.date.accessioned2010-07-07T23:45:15Z-
dc.date.available2010-07-07T23:45:15Z-
dc.date.issued2007-07-31-
dc.identifier.citationCardiovasc Res. 2007;76(2):224-235en
dc.identifier.issn0008-6363 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17658500-
dc.identifier.urihttps://hdl.handle.net/10371/68478-
dc.description.abstractOBJECTIVE: The mechanosensitive nonselective cation channel (NSC(MS)) and endothelin-1 (ET-1) play critical roles in the regulation of vascular tone. This study was undertaken to investigate the effect of ET-1 on NSC(MS) and on the myogenic response of arteries. METHODS: Cell-attached patch-clamp techniques were applied to rabbit pulmonary and cerebral arterial smooth muscle cells using a 140 mM CsCl pipette and bath solutions (Ca(2+)-free, 1 mM EGTA). Myogenic responses were determined by video analysis of pressurized arteries. RESULTS: The application of negative pressures through the pipette activated NSC(MS), and this was augmented by bath application of ET-1 (1 pM-30 nM). ET-1 lowered the lowest pressure required for NSC(MS) activation. NSC(MS) facilitation by ET-1 was prevented by BQ-123 (1 microM, an ET(A) antagonist) but not by BQ-788 (1 microM, an ET(B) antagonist). Phorbol 12-myristate 13-acetate (PMA, 100 nM), a protein kinase C activator, also increased the activity of NSC(MS). ET-1- or PMA-induced facilitation of NSC(MS) was abolished by GF109203X (10 microM), a protein kinase C inhibitor. Video analysis of pressurized cerebral artery showed inhibition of the myogenic response by the NSC(MS) channel blockers GsMTx-4 (5 microM) and DIDS (3-100 microM). Treatment with ET-1 (10 pM) augmented the myogenic response and this was inhibited by DIDS (30 microM). CONCLUSION: Stimulation of ET-1 receptor (ET(A)) facilitates NSC(MS) via a protein kinase C-dependent signaling pathway in rabbit arterial myocytes. Our findings suggest that NSC(MS) play a role in the myogenic response and its augmentation by ET-1.en
dc.description.sponsorshipThis work was supported by the Korea Research Foundation
funded by theKoreanGovernment (MOEHRD, Basic Research
Promotion Fund, KRF-2006-E00021).
en
dc.language.isoenen
dc.publisherElsevieren
dc.subjectAnimalsen
dc.subjectCalcium/metabolismen
dc.subjectEndothelin-1/*pharmacologyen
dc.subjectFemaleen
dc.subjectHumansen
dc.subjectMaleen
dc.subjectMuscle, Smooth, Vascular/cytology/*drug effects/physiologyen
dc.subjectMyocytes, Smooth Muscle/*drug effects/physiologyen
dc.subjectPeptides/pharmacologyen
dc.subjectProtein Kinase C/*physiologyen
dc.subjectPulmonary Artery/cytology/drug effects/physiologyen
dc.subjectRabbitsen
dc.subjectSpider Venoms/pharmacologyen
dc.subjectStress, Mechanicalen
dc.subjectTRPC Cation Channels/drug effects/physiologyen
dc.subjectTRPM Cation Channels/drug effects/physiologyen
dc.subjectTransient Receptor Potential Channels/*drug effects/physiologyen
dc.titleMechanosensitive nonselective cation channel facilitation by endothelin-1 is regulated by protein kinase C in arterial myocytesen
dc.typeArticleen
dc.contributor.AlternativeAuthor이향애-
dc.contributor.AlternativeAuthor백은복-
dc.contributor.AlternativeAuthor박경선-
dc.contributor.AlternativeAuthor정회종-
dc.contributor.AlternativeAuthor김재일-
dc.contributor.AlternativeAuthor김성준-
dc.contributor.AlternativeAuthor엄융의-
dc.identifier.doi10.1016/j.cardiores.2007.06.021-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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