| Oleic acid inhibits endothelial nitric oxide synthase by a protein kinase C-independent mechanism. | |
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MedLine Citation:
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PMID: 7591016 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Many obese hypertensive individuals have a cluster of cardiovascular risk factors. This cluster includes plasma nonesterified fatty acid concentrations and turnover rates that are higher and more resistant to suppression by insulin than in lean and obese normotensive individuals. The higher fatty acids may contribute to cardiovascular risk in these patients by inhibiting endothelial cell nitric oxide synthase activity. To test this hypothesis, we quantified the effects of oleic (18:1[cis]) and other 18-carbon fatty acids on nitric oxide synthase activity in cultured bovine pulmonary artery endothelial cells by measuring the conversion of [3H]L-arginine to [3H]L-citrulline. Oleic acid (from 10 to 100 mumol/L) caused a concentration-dependent decrease in nitric oxide synthase activity at baseline and during ATP and ionomycin (Ca2+ ionophore) stimulation. At 100 mumol/L, linoleic (18:2[cis]) and oleic acids caused similar reductions of nitric oxide synthase activity, whereas elaidic (18:1[trans]) and stearic (18:0) acids had no effect. Oleic acid also inhibited the endothelium-dependent vasodilator response to acetylcholine in rabbit femoral artery rings preconstricted with phenylephrine (P < .05) but had no effect on the response to nitroprusside. The pattern of 18-carbon fatty acid effects on nitric oxide synthase activity in endothelial cells is consistent with activation of protein kinase C. Although oleic acid increased protein kinase C activity in endothelial cells, neither depletion of protein kinase C by 24-hour pretreatment with phorbol 12-myristate 13-acetate nor its inhibition with staurosporine eliminated the inhibitory effect of oleic acid on nitric oxide synthase.(ABSTRACT TRUNCATED AT 250 WORDS) |
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Authors:
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R K Davda; K T Stepniakowski; G Lu; M E Ullian; T L Goodfriend; B M Egan |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Hypertension Volume: 26 ISSN: 0194-911X ISO Abbreviation: Hypertension Publication Date: 1995 Nov |
Date Detail:
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Created Date: 1995-12-07 Completed Date: 1995-12-07 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 764-70 Citation Subset: IM |
Affiliation:
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Division of Nephrology, Medical University of South Carolina, Charleston 29425-2251, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cattle Cells, Cultured Endothelium, Vascular / metabolism* Enzyme Activation / drug effects Femoral Artery / drug effects, physiology Humans Hypertension / metabolism Nitric Oxide Synthase / antagonists & inhibitors* Oleic Acid Oleic Acids / blood, pharmacology* Protein Kinase C / metabolism* Rabbits Vasodilation / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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R01-43164//PHS HHS |
| Chemical | |
Reg. No./Substance:
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0/Oleic Acids; 112-80-1/Oleic Acid; EC 1.14.13.39/Nitric Oxide Synthase; 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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