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Article: Increases in flow reduce the release of endothelium-derived relaxing factor in the aorta of normotensive and spontaneously hypertensive rats

TitleIncreases in flow reduce the release of endothelium-derived relaxing factor in the aorta of normotensive and spontaneously hypertensive rats
Authors
KeywordsAcetylcholine
Aorta
EDRF
Flow
In vitro
SHR
WKY
Issue Date1989
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyper
Citation
American Journal Of Hypertension, 1989, v. 2 n. 10, p. 762-767 How to Cite?
AbstractExperiments were designed to compare basal and acetylcholine-induced release of endothelium-derived relaxing factor at different flow rates in the aorta of the normotensive (Wistar-Kyoto; WKY) and spontaneously hypertensive (SHR) rat. Aortic segments (with endothelium) of either WKY or SHR were perfused at different flow rates (1 or 4 mL/min) with modified Krebs-Ringer solution; the relaxing activity of the perfusate from the two types of segments was bioassayed by measuring the isometric force in rings (without endothelium, and contracted with norepinephrine) of aortas of both WKY and SHR. All studies were performed in the presence of indomethacin to prevent endothelial production of prostacyclin and other vasodilator prostanoids. The basal release of endothelium-derived relaxing factor was not significantly affected by the flow rate in either the WKY or the SHR aortas. At the two flow rates, and with both types of bioassay rings, the basal release of endothelium-derived relaxing factor was smaller with SHR than with WKY aortas, but this reached significance only at 4 mL/min using the SHR-aorta as bioassay tissue. Both with WKY and SHR aortas the release of endothelium-derived relaxing factor evoked by acetylcholine was significantly larger at 1 than at 4 mL/min; no significant differences in responsiveness to acetylcholine were noted between WKY and SHR segments. There was also no difference in responsiveness of WKY and SHR bioassay rings to acetylcholine and acetylcholine-induced release of endothelium-derived relaxing factor. These experiments suggest that prolonged exposure to increases in shear stress reduced the ability of the endothelium to release endothelium-derived relaxing factor in responses to muscarinic activation.
Persistent Identifierhttp://hdl.handle.net/10722/170935
ISSN
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 0.925
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHoeffner, Uen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:30Z-
dc.date.available2012-10-30T06:11:30Z-
dc.date.issued1989en_US
dc.identifier.citationAmerican Journal Of Hypertension, 1989, v. 2 n. 10, p. 762-767en_US
dc.identifier.issn0895-7061en_US
dc.identifier.urihttp://hdl.handle.net/10722/170935-
dc.description.abstractExperiments were designed to compare basal and acetylcholine-induced release of endothelium-derived relaxing factor at different flow rates in the aorta of the normotensive (Wistar-Kyoto; WKY) and spontaneously hypertensive (SHR) rat. Aortic segments (with endothelium) of either WKY or SHR were perfused at different flow rates (1 or 4 mL/min) with modified Krebs-Ringer solution; the relaxing activity of the perfusate from the two types of segments was bioassayed by measuring the isometric force in rings (without endothelium, and contracted with norepinephrine) of aortas of both WKY and SHR. All studies were performed in the presence of indomethacin to prevent endothelial production of prostacyclin and other vasodilator prostanoids. The basal release of endothelium-derived relaxing factor was not significantly affected by the flow rate in either the WKY or the SHR aortas. At the two flow rates, and with both types of bioassay rings, the basal release of endothelium-derived relaxing factor was smaller with SHR than with WKY aortas, but this reached significance only at 4 mL/min using the SHR-aorta as bioassay tissue. Both with WKY and SHR aortas the release of endothelium-derived relaxing factor evoked by acetylcholine was significantly larger at 1 than at 4 mL/min; no significant differences in responsiveness to acetylcholine were noted between WKY and SHR segments. There was also no difference in responsiveness of WKY and SHR bioassay rings to acetylcholine and acetylcholine-induced release of endothelium-derived relaxing factor. These experiments suggest that prolonged exposure to increases in shear stress reduced the ability of the endothelium to release endothelium-derived relaxing factor in responses to muscarinic activation.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyperen_US
dc.relation.ispartofAmerican Journal of Hypertensionen_US
dc.subjectAcetylcholine-
dc.subjectAorta-
dc.subjectEDRF-
dc.subjectFlow-
dc.subjectIn vitro-
dc.subjectSHR-
dc.subjectWKY-
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Metabolismen_US
dc.subject.meshBlood Circulationen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshStimulation, Chemicalen_US
dc.subject.meshVasoconstrictionen_US
dc.subject.meshVasodilationen_US
dc.titleIncreases in flow reduce the release of endothelium-derived relaxing factor in the aorta of normotensive and spontaneously hypertensive ratsen_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.doi10.1093/ajh/2.10.762-
dc.identifier.pmid2803671-
dc.identifier.scopuseid_2-s2.0-0024423081en_US
dc.identifier.volume2en_US
dc.identifier.issue10en_US
dc.identifier.spage762en_US
dc.identifier.epage767en_US
dc.identifier.isiWOS:A1989AR65300004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHoeffner, U=7801661618en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.issnl0895-7061-

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