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Article: A diffusible substance(s) mediates endothelium-dependent contractions in the aorta of SHR

TitleA diffusible substance(s) mediates endothelium-dependent contractions in the aorta of SHR
Authors
KeywordsCyclooxygenase
Endothelium-dependent contraction
Free radicals
Rats, spontaneously hypertensive
Receptors, thromboxane
Tetrahydrobiopterin
Issue Date2003
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 2003, v. 41 n. 1, p. 143-148 How to Cite?
AbstractA modified bioassay system was designed to demonstrate the diffusible nature of endothelium-derived contracting factor(s) released by acetylcholine in the aorta of spontaneously hypertensive rat. In "sandwich"-like layered preparation, isometric tension was recorded from a bioassay strip (without endothelium) in the presence of NG-nitro-L-arginine and tetrahydrobiopterin to selectively potentiate endothelium-dependent contractions. A donor strip (with or without endothelium) was stitched on the bioassay tissue so that it did not directly contribute to the recorded contractions. Acetylcholine induced contractions that occurred only when the donor strip was with endothelium. Superoxide dismutase did not affect but catalase and the combination of superoxide dismutase plus catalase significantly decreased the endothelium-dependent contraction. The contractions in the layered preparations were abolished when the donor strip with endothelium was treated previously with valeryl salicylate, an irreversible cyclooxygenase-1 inhibitor, but remained unaffected when the bioassay strip was treated with the compound. Previous treatment of the bioassay strip alone with S 18886 abolished the contractile response, whereas treatment of the donor strip with endothelium by the selective TP receptor antagonist only produced a moderate inhibition. These results indicate that in the aorta of spontaneously hypertensive rats, endothelium-dependent contractions to acetylcholine involve a diffusible substance(s) released by the endothelium. The production of this contracting factor(s) requires the activation of endothelial cyclooxygenase-1, and its action the activation of TP receptors on the vascular smooth muscle cells.
Persistent Identifierhttp://hdl.handle.net/10722/171288
ISSN
2023 Impact Factor: 6.9
2023 SCImago Journal Rankings: 2.827
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, Den_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorLevens, Nen_US
dc.contributor.authorZhang, JNen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:12Z-
dc.date.available2012-10-30T06:13:12Z-
dc.date.issued2003en_US
dc.identifier.citationHypertension, 2003, v. 41 n. 1, p. 143-148en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171288-
dc.description.abstractA modified bioassay system was designed to demonstrate the diffusible nature of endothelium-derived contracting factor(s) released by acetylcholine in the aorta of spontaneously hypertensive rat. In "sandwich"-like layered preparation, isometric tension was recorded from a bioassay strip (without endothelium) in the presence of NG-nitro-L-arginine and tetrahydrobiopterin to selectively potentiate endothelium-dependent contractions. A donor strip (with or without endothelium) was stitched on the bioassay tissue so that it did not directly contribute to the recorded contractions. Acetylcholine induced contractions that occurred only when the donor strip was with endothelium. Superoxide dismutase did not affect but catalase and the combination of superoxide dismutase plus catalase significantly decreased the endothelium-dependent contraction. The contractions in the layered preparations were abolished when the donor strip with endothelium was treated previously with valeryl salicylate, an irreversible cyclooxygenase-1 inhibitor, but remained unaffected when the bioassay strip was treated with the compound. Previous treatment of the bioassay strip alone with S 18886 abolished the contractile response, whereas treatment of the donor strip with endothelium by the selective TP receptor antagonist only produced a moderate inhibition. These results indicate that in the aorta of spontaneously hypertensive rats, endothelium-dependent contractions to acetylcholine involve a diffusible substance(s) released by the endothelium. The production of this contracting factor(s) requires the activation of endothelial cyclooxygenase-1, and its action the activation of TP receptors on the vascular smooth muscle cells.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_US
dc.relation.ispartofHypertensionen_US
dc.subjectCyclooxygenase-
dc.subjectEndothelium-dependent contraction-
dc.subjectFree radicals-
dc.subjectRats, spontaneously hypertensive-
dc.subjectReceptors, thromboxane-
dc.subjectTetrahydrobiopterin-
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Drug Effects - Physiopathologyen_US
dc.subject.meshBiological Assay - Methodsen_US
dc.subject.meshBiopterin - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshCyclooxygenase 1en_US
dc.subject.meshDiffusionen_US
dc.subject.meshEndothelium, Vascular - Chemistry - Enzymology - Physiopathologyen_US
dc.subject.meshHypertension - Enzymology - Metabolism - Physiopathologyen_US
dc.subject.meshIsoenzymes - Analysis - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Proteinsen_US
dc.subject.meshMuscle, Smooth, Vascular - Chemistryen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Analysis - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshReceptors, Thromboxane - Analysis - Physiologyen_US
dc.subject.meshVasoconstrictionen_US
dc.subject.meshVasoconstrictor Agents - Analysis - Pharmacologyen_US
dc.titleA diffusible substance(s) mediates endothelium-dependent contractions in the aorta of SHRen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1161/01.HYP.0000047651.45322.16en_US
dc.identifier.pmid12511544-
dc.identifier.scopuseid_2-s2.0-0037219457en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037219457&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume41en_US
dc.identifier.issue1en_US
dc.identifier.spage143en_US
dc.identifier.epage148en_US
dc.identifier.isiWOS:000180367000024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridYang, D=7404801018en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridLevens, N=7006081223en_US
dc.identifier.scopusauthoridZhang, JN=7601344287en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0194-911X-

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