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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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Authors
Lee, Hyang Ae; Baek, Eun Bok; Park, Kyung Sun; Jung, Hoi Jong; Kim, Jae Il; Kim, Sung Joon; Earm, Yung E
Issue Date
2007-07-31
Publisher
Elsevier
Citation
Cardiovasc Res. 2007;76(2):224-235
Keywords
AnimalsCalcium/metabolismEndothelin-1/*pharmacologyFemaleHumansMaleMuscle, Smooth, Vascular/cytology/*drug effects/physiologyMyocytes, Smooth Muscle/*drug effects/physiologyPeptides/pharmacologyProtein Kinase C/*physiologyPulmonary Artery/cytology/drug effects/physiologyRabbitsSpider Venoms/pharmacologyStress, MechanicalTRPC Cation Channels/drug effects/physiologyTRPM Cation Channels/drug effects/physiologyTransient Receptor Potential Channels/*drug effects/physiology
Abstract
OBJECTIVE: 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.
ISSN
0008-6363 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17658500

http://hdl.handle.net/10371/68478
DOI
https://doi.org/10.1016/j.cardiores.2007.06.021
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
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