| Pulsatile mechanical pressure promotes Angiotensin-converting enzyme expression in aortic smooth muscle cells. | |
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MedLine Citation:
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PMID: 18679784 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Hypertension is a major risk factor for atherosclerosis, and elevated pressure (i.e., mechanical pressure stresses) has been known to modulate vascular remodeling, possibly by affecting the tissue renin-angiotensin system. METHODS: In the present study we applied pulsatile pressure to human aortic smooth muscle cells (HASMCs) and investigated whether mechanical pressure stress affects cell proliferation and/or the angiotensin-converting enzyme (ACE), and we tested whether the administration of an angiotensin II (AII) receptor blocker has a favorable effect. RESULTS: Three hours of pulsatile atmospheric pressure resulted in an approximately 8% increase in cell proliferation of human aortic smooth muscle cells. The cell surface ACE level, enzyme activity and mRNA expression were all elevated (37%, 110% and 17%, respectively) under pressurized conditions, and co-administration of AII reduced all these values. The reductions in these three parameters resulting from the administration of AII were all abolished by AII receptor blocker co-administration and values were increased (11%, 62% and 12%, respectively) under pressurized conditions. Pulsatile atmospheric pressure increased the amount of phosphorylated extracellular signal-regulated kinase (ERK) by approximately 54% in HASMCs. The administration of PD98059 (10 microM) resulted in a decrease in phosphorylated ERK and ACE activity in HASMCs compared to those of the pressurized control. CONCLUSION: From these observations, we conclude that pulsatile mechanical pressure is one of the mediators of ACE production in vascular smooth muscle cells and that AII receptor blocking may prevent negative feedback. The present findings may provide a potential therapeutical target beyond lowering blood pressure in hypertensive patients. |
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Authors:
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Kenji Iizuka; Takuji Machida; Hideaki Kawaguchi; Masahiko Hirafuji |
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Publication Detail:
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Type: Journal Article Date: 2008-08-05 |
Journal Detail:
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Title: Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy Volume: 22 ISSN: 0920-3206 ISO Abbreviation: Cardiovasc Drugs Ther Publication Date: 2008 Oct |
Date Detail:
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Created Date: 2008-09-05 Completed Date: 2009-01-12 Revised Date: 2013-06-03 |
Medline Journal Info:
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Nlm Unique ID: 8712220 Medline TA: Cardiovasc Drugs Ther Country: United States |
Other Details:
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Languages: eng Pagination: 383-90 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido, 061-0293, Japan. kiizuka@hoku-iryo-u.ac.jp |
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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pharmacology Angiotensin Receptor Antagonists Aorta / cytology Atmospheric Pressure Benzimidazoles / pharmacology Captopril / pharmacology Cell Line Cell Proliferation / drug effects Colorimetry / methods Dose-Response Relationship, Drug Extracellular Signal-Regulated MAP Kinases / metabolism Flavonoids / pharmacology Gene Expression Regulation, Enzymologic / drug effects Humans Immunoblotting Membrane Proteins / genetics, metabolism Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors, metabolism Muscle, Smooth, Vascular / cytology, drug effects, metabolism* Peptidyl-Dipeptidase A / genetics*, metabolism* Phosphorylation / drug effects RNA, Messenger / genetics, metabolism Reverse Transcriptase Polymerase Chain Reaction Stress, Mechanical Tetrazoles / pharmacology Time Factors |
| Chemical | |
Reg. No./Substance:
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0/2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0/Angiotensin Receptor Antagonists; 0/Benzimidazoles; 0/Flavonoids; 0/Membrane Proteins; 0/RNA, Messenger; 0/Tetrazoles; 11128-99-7/Angiotensin II; 62571-86-2/Captopril; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 3.4.15.1/Peptidyl-Dipeptidase A; S8Q36MD2XX/candesartan |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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