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Article: Enhanced production of nitric oxide in aortae from spontaneously hypertensive rats by interleukin-1β

TitleEnhanced production of nitric oxide in aortae from spontaneously hypertensive rats by interleukin-1β
Authors
Issue Date1993
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyper
Citation
American Journal Of Hypertension, 1993, v. 6 n. 7 I, p. 602-610 How to Cite?
AbstractCultured aortic smooth muscle cells from spontaneously hypertensive rats produce more nitrite than cells from Wistar-Kyoto rats in response to interleukin-1β. Therefore, the effect of interleukin-1β-induced nitric oxide production was compared on the contractility of aortic smooth muscle from spontaneously hypertensive and Wistar-Kyoto rats. Under control conditions, there was no difference in the response of aortic rings (without endothelium) to phenylephrine between both strains. Contractions to 5-hydroxytryptamine were larger in preparations from hypertensive than normotensive animals. Treatment with interleukin-1β for 6 h reduced the responsiveness to both vasoconstrictors in a concentration-dependent manner. The depression was more pronounced in rings from spontaneously hypertensive rats: the threshold concentration of the cytokine was lower, and its maximal effect greater. Nitro-L-arginine prevented the inhibitory effect of interleukin-1β. The cytokine evoked a time-dependent loss of tone in phenylephrine-contracted rings with the same time of onset in both strains. However, the decay of tension was more pronounced in aortae from hypertensive than normotensive rats. In aortae from both strains, the decay was potentiated by L-arginine, but not D-arginine. Interleukin-1β elicited greater concentration-dependent productions of cyclic GMP and nitrite in rings from spontaneously hypertensive than from Wistar-Kyoto rats, and these were inhibited by methylene blue and nitro-L-arginine, respectively. The concentration-relaxation curves to 3-morpholino-sydnonimine were moderately, but significantly, shifted to the left in aortae from spontaneously hypertensive rats. These data suggest that interleukin-1β induces a greater production of nitric oxide in aortic smooth muscle from spontaneously hypertensive than Wistar-Kyoto rats. This results in a higher and long-lasting activation of soluble guanylate cyclase, which in turn impairs contractility of vascular smooth muscle to a larger extent in the hypertensive strain.
Persistent Identifierhttp://hdl.handle.net/10722/171084
ISSN
2015 Impact Factor: 3.182
2015 SCImago Journal Rankings: 1.397
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJunquero, DCen_US
dc.contributor.authorSchini, VBen_US
dc.contributor.authorScottBurden, Ten_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:08Z-
dc.date.available2012-10-30T06:12:08Z-
dc.date.issued1993en_US
dc.identifier.citationAmerican Journal Of Hypertension, 1993, v. 6 n. 7 I, p. 602-610en_US
dc.identifier.issn0895-7061en_US
dc.identifier.urihttp://hdl.handle.net/10722/171084-
dc.description.abstractCultured aortic smooth muscle cells from spontaneously hypertensive rats produce more nitrite than cells from Wistar-Kyoto rats in response to interleukin-1β. Therefore, the effect of interleukin-1β-induced nitric oxide production was compared on the contractility of aortic smooth muscle from spontaneously hypertensive and Wistar-Kyoto rats. Under control conditions, there was no difference in the response of aortic rings (without endothelium) to phenylephrine between both strains. Contractions to 5-hydroxytryptamine were larger in preparations from hypertensive than normotensive animals. Treatment with interleukin-1β for 6 h reduced the responsiveness to both vasoconstrictors in a concentration-dependent manner. The depression was more pronounced in rings from spontaneously hypertensive rats: the threshold concentration of the cytokine was lower, and its maximal effect greater. Nitro-L-arginine prevented the inhibitory effect of interleukin-1β. The cytokine evoked a time-dependent loss of tone in phenylephrine-contracted rings with the same time of onset in both strains. However, the decay of tension was more pronounced in aortae from hypertensive than normotensive rats. In aortae from both strains, the decay was potentiated by L-arginine, but not D-arginine. Interleukin-1β elicited greater concentration-dependent productions of cyclic GMP and nitrite in rings from spontaneously hypertensive than from Wistar-Kyoto rats, and these were inhibited by methylene blue and nitro-L-arginine, respectively. The concentration-relaxation curves to 3-morpholino-sydnonimine were moderately, but significantly, shifted to the left in aortae from spontaneously hypertensive rats. These data suggest that interleukin-1β induces a greater production of nitric oxide in aortic smooth muscle from spontaneously hypertensive than Wistar-Kyoto rats. This results in a higher and long-lasting activation of soluble guanylate cyclase, which in turn impairs contractility of vascular smooth muscle to a larger extent in the hypertensive strain.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.subject.meshAnimalsen_US
dc.subject.meshAorta - Drug Effects - Metabolismen_US
dc.subject.meshCulture Techniquesen_US
dc.subject.meshCyclic Gmp - Biosynthesisen_US
dc.subject.meshInterleukin-1 - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshNitrites - Metabolismen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshSerotonin - Pharmacologyen_US
dc.titleEnhanced production of nitric oxide in aortae from spontaneously hypertensive rats by interleukin-1βen_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/6.7.602-
dc.identifier.pmid8398001-
dc.identifier.scopuseid_2-s2.0-0027213759en_US
dc.identifier.volume6en_US
dc.identifier.issue7 Ien_US
dc.identifier.spage602en_US
dc.identifier.epage610en_US
dc.identifier.isiWOS:A1993LP44000008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridJunquero, DC=26643025500en_US
dc.identifier.scopusauthoridSchini, VB=7004113565en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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