| Reduced endothelium-dependent relaxation at enhanced NO release in hearts of hypercholesterolaemic rabbits. | |
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MedLine Citation:
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PMID: 8032587 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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1. Langendorff hearts, perfused at constant volume, were prepared from rabbits fed a cholesterol-enriched diet for 4 months. Coronary perfusion pressure and nitric oxide (NO) release (oxyhaemoglobin technique) into the coronary effluent were measured continuously. Prostacyclin (PGI2) in the effluents was determined by radioimmunoassay (6-oxo-PGF1 alpha). 2. Basal NO release was not different between control and hypercholesterolaemic rabbits. However, the coronary vasculature of hypercholesterolaemic rabbits showed a considerably (> 50%) reduced endothelium-dependent relaxation in response to short-term (3 min) infusion of bradykinin (50 nM) and substance P (50 nM) (P < 0.05, n = 8-9). Under these conditions, NO release into the vessel lumen was increased, by 26%, in hypercholesterolaemic hearts (P < 0.05, n = 8-9). NG-nitro-L-arginine (L-NOARG, 30 microM) significantly attenuated both bradykinin-induced NO formation and vessel relaxation in control hearts but only NO release in hypercholesterolaemia. L-Arginine (200 microM) restored the response to that before L-NOARG but did not improve the reduced endothelium-dependent relaxation in cholesterol-fed rabbits. 3. Superoxide dismutase (10 u ml-1) significantly improved vessel relaxation without changing the hypercholesterolaemia-related coronary dysfunction. Vasodilatation in response to exogenous NO donors (linsidomine) was diminished in hypercholesterolaemia as compared to controls. 4. Basal PGI2 release was unchanged in hypercholesterolaemic hearts. There was a tendency in these hearts for greater PGI2 formation after stimulation by substance P and bradykinin (P > or = 0.05). The coronary relaxation to iloprost was unchanged. 5. The data demonstrate impaired endothelium-dependent relaxation of coronary arterial resistance vessels in hypercholesterolaemia. This diminished vascular response was not due to reduced NO generation but probably a reduced action of released NO, either by accelerated degradation and/or disturbed signal transduction pathways to vascular smooth muscle cells. There was no significant change in PGI2 related pathways of vasomotor control in hypercholesterolaemia. |
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Authors:
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I Woditsch; K Schrör |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: British journal of pharmacology Volume: 111 ISSN: 0007-1188 ISO Abbreviation: Br. J. Pharmacol. Publication Date: 1994 Apr |
Date Detail:
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Created Date: 1994-08-17 Completed Date: 1994-08-17 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 1035-40 Citation Subset: IM |
Affiliation:
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Institut für Pharmakologie, Heinrich-Heine-Universität Düsseldorf, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arginine / analogs & derivatives, pharmacology Coronary Vessels / physiopathology* Endothelium, Vascular / physiology* Epoprostenol / biosynthesis Hypercholesterolemia / physiopathology* Myocardium / metabolism* Nitric Oxide / metabolism* Nitroarginine Rabbits Superoxide Dismutase / pharmacology Vasodilation* |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine; 35121-78-9/Epoprostenol; 74-79-3/Arginine; EC 1.15.1.1/Superoxide Dismutase |
| Comments/Corrections | |
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