| Converting enzyme inhibitor temocaprilat prevents high glucose-mediated suppression of human aortic endothelial cell proliferation. | |
MedLine Citation:
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PMID: 14871030 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We examined the involvement of the oxidative stress in high glucose-induced suppression of human aortic endothelial cell proliferation. Chronic glucose treatment for 72 h concentration-dependently (5.6-22.2 mol/l) inhibited human coronary endothelial cell proliferation. Temocaprilat, an angiotensin-converting enzyme inhibitor, at 10 nmol/l to 1 micromol/l inhibited high glucose (22.2 mmol/l)-mediated suppression of human aortic endothelial cell proliferation. Temocaprilat at 1 micromol/l inhibited high glucose-induced membrane-bound protein kinase C activity in human aortic endothelial cells. The protein kinase C inhibitors calphostin C 100 nmol/l or chelerythrine 1 micromol/l inhibited high glucose-mediated suppression of human aortic endothelial cell proliferation. Chronic high glucose treatment for 72 h increased intracellular oxidative stress, directly measured by flow cytometry using carboxydichlorofluorescein diacetate bis-acetoxymethyl ester, and this increase was significantly suppressed by temocaprilat 10 nmol/l to 1 micromol/l. Bradykinin B2 receptor antagonist icatibant 100 nmol/l significantly reduced the action of temocaprilat; whereas bradykinin B1 receptor antagonist des-Arg9-Leu8-bradykinin 100 nmol/l had no effect. These findings suggest that high glucose inhibits human aortic endothelial cell proliferation and that the angiotensin-converting enzyme inhibitor temocaprilat inhibits high glucose-mediated suppression of human aortic endothelial cell proliferation, possibly through suppression of protein kinase C, bradykinin B2 receptors and oxidative stress. |
Authors:
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Kenichi Yasunari; Kensaku Maeda; Takanori Watanabe; Munehiro Nakamura; Akira Asada; Junichi Yoshikawa |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cardiovascular pharmacology Volume: 42 Suppl 1 ISSN: 0160-2446 ISO Abbreviation: J. Cardiovasc. Pharmacol. Publication Date: 2003 Dec |
Date Detail:
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Created Date: 2004-02-11 Completed Date: 2004-03-30 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7902492 Medline TA: J Cardiovasc Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: S55-60 Citation Subset: IM |
Affiliation:
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Department of General Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan. yasunari@osaka-med.or.jp |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Alkaloids Angiotensin-Converting Enzyme Inhibitors / administration & dosage, pharmacokinetics* Aorta / cytology*, drug effects*, metabolism Benzophenanthridines Bradykinin / analogs & derivatives*, antagonists & inhibitors Cell Division / drug effects*, physiology Cell Membrane / enzymology Cells, Cultured Coronary Vessels / cytology Dose-Response Relationship, Drug Endothelial Cells / drug effects*, enzymology, metabolism Glucose / administration & dosage, adverse effects, antagonists & inhibitors* Humans Naphthalenes / administration & dosage, pharmacokinetics Oxidative Stress / drug effects, physiology Phenanthridines / administration & dosage, pharmacokinetics Protein Kinase C / antagonists & inhibitors, drug effects, metabolism Receptor, Bradykinin B1 / administration & dosage, physiology Receptor, Bradykinin B2 / antagonists & inhibitors, physiology Thiazepines / pharmacology* Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Alkaloids; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Benzophenanthridines; 0/Naphthalenes; 0/Phenanthridines; 0/Receptor, Bradykinin B1; 0/Receptor, Bradykinin B2; 0/Thiazepines; 110221-53-9/temocaprilat; 121263-19-2/calphostin C; 130308-48-4/icatibant; 34316-15-9/chelerythrine; 50-99-7/Glucose; 58-82-2/Bradykinin; 64695-06-3/bradykinin, Leu(8)-des-Arg(9)-; EC 2.7.11.13/Protein Kinase C |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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