Document Detail


Converting enzyme inhibitor temocaprilat prevents high glucose-mediated suppression of human aortic endothelial cell proliferation.
MedLine Citation:
PMID:  14871030     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Kenichi Yasunari; Kensaku Maeda; Takanori Watanabe; Munehiro Nakamura; Akira Asada; Junichi Yoshikawa
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  42 Suppl 1     ISSN:  0160-2446     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2003 Dec 
Date Detail:
Created Date:  2004-02-11     Completed Date:  2004-03-30     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  S55-60     Citation Subset:  IM    
Affiliation:
Department of General Medicine, Osaka City University Graduate School of Medicine, Osaka, Japan. yasunari@osaka-med.or.jp
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MeSH Terms
Descriptor/Qualifier:
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:
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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