File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Endothelium-dependent responses in carotid and renal arteries of normotensive and hypertensive rats

TitleEndothelium-dependent responses in carotid and renal arteries of normotensive and hypertensive rats
Authors
KeywordsAcetylcholine
Adenosine 5′-diphosphate
Indomethacin
Prostaglandins
Serotonin
Sodium nitroprusside
Spontaneously hypertensive rats
Wistar-kyoto rats
Issue Date1988
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1988, v. 11 n. 6 PART 2, p. 573-578 How to Cite?
AbstractEndothelium-dependent relaxations are impaired in the aorta of various models of hypertension, but no data are available regarding the cerebral or renal circulation. Endothelium-dependent relaxations were studied in the carotid and renal artery of Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Rings with and without endothelium were suspended in organ chambers for isometric tension recording. Acetylcholine and adenosine 5'-diphosphate (ADP) caused endothelium-dependent relaxations in both arteries that were impaired in the carotid, but not in the renal artery, of the SHR, similar to those to the endothelium-independent vasodilator sodium nitroprusside. Indomethacin did not affect relaxations to acetylcholine in the carotid artery, but it significantly augmented them in the renal artery. This finding suggests that an impaired vascular responsiveness to endothelium-derived relaxing factor is responsible for the decreased relaxations in the carotid artery of the SHR. In the renal artery, acetylcholine appears to release both endothelium-derived relaxing factor and a vasoconstrictor prostanoid. Carotid arteries of SHR were more sensitive to the constrictor effects of serotonin than were those of WKY. Endothelium removal caused a twofold to eightfold increase in sensitivity to serotonin in both strains. Thus, the endothelium-dependent relaxations to acetylcholine and ADP are reduced and constrictions to serotonin are enhanced in the carotid, but not in the renal, artery of the SHR.
Persistent Identifierhttp://hdl.handle.net/10722/170875
ISSN
2021 Impact Factor: 9.897
2020 SCImago Journal Rankings: 2.986
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLuscher, TFen_US
dc.contributor.authorDiederich, Den_US
dc.contributor.authorWeber, Een_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBuhler, FRen_US
dc.date.accessioned2012-10-30T06:11:14Z-
dc.date.available2012-10-30T06:11:14Z-
dc.date.issued1988en_US
dc.identifier.citationHypertension, 1988, v. 11 n. 6 PART 2, p. 573-578en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170875-
dc.description.abstractEndothelium-dependent relaxations are impaired in the aorta of various models of hypertension, but no data are available regarding the cerebral or renal circulation. Endothelium-dependent relaxations were studied in the carotid and renal artery of Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Rings with and without endothelium were suspended in organ chambers for isometric tension recording. Acetylcholine and adenosine 5'-diphosphate (ADP) caused endothelium-dependent relaxations in both arteries that were impaired in the carotid, but not in the renal artery, of the SHR, similar to those to the endothelium-independent vasodilator sodium nitroprusside. Indomethacin did not affect relaxations to acetylcholine in the carotid artery, but it significantly augmented them in the renal artery. This finding suggests that an impaired vascular responsiveness to endothelium-derived relaxing factor is responsible for the decreased relaxations in the carotid artery of the SHR. In the renal artery, acetylcholine appears to release both endothelium-derived relaxing factor and a vasoconstrictor prostanoid. Carotid arteries of SHR were more sensitive to the constrictor effects of serotonin than were those of WKY. Endothelium removal caused a twofold to eightfold increase in sensitivity to serotonin in both strains. Thus, the endothelium-dependent relaxations to acetylcholine and ADP are reduced and constrictions to serotonin are enhanced in the carotid, but not in the renal, artery of the SHR.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.subjectAcetylcholine-
dc.subjectAdenosine 5′-diphosphate-
dc.subjectIndomethacin-
dc.subjectProstaglandins-
dc.subjectSerotonin-
dc.subjectSodium nitroprusside-
dc.subjectSpontaneously hypertensive rats-
dc.subjectWistar-kyoto rats-
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdenosine Diphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Agents - Physiologyen_US
dc.subject.meshCarotid Arteries - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshIsometric Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiopathologyen_US
dc.subject.meshNitric Oxideen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shr - Physiologyen_US
dc.subject.meshRats, Inbred Strains - Physiologyen_US
dc.subject.meshRats, Inbred Wky - Physiologyen_US
dc.subject.meshRenal Artery - Physiopathologyen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.titleEndothelium-dependent responses in carotid and renal arteries of normotensive and 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.doi10.1161/01.HYP.11.6.573-
dc.identifier.pmid3260580-
dc.identifier.scopuseid_2-s2.0-0023755072en_US
dc.identifier.volume11en_US
dc.identifier.issue6 PART 2en_US
dc.identifier.spage573en_US
dc.identifier.epage578en_US
dc.identifier.isiWOS:A1988P204500003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLuscher, TF=18935805600en_US
dc.identifier.scopusauthoridDiederich, D=7004821557en_US
dc.identifier.scopusauthoridWeber, E=7401971488en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBuhler, FR=8838192300en_US
dc.identifier.issnl0194-911X-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats