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dc.contributor.authorAngeli, Jully Kelypt_BR
dc.contributor.authorRamos, Denise Barbosapt_BR
dc.contributor.authorCasali, Emerson Andrept_BR
dc.contributor.authorSouza, Diogo Onofre Gomes dept_BR
dc.contributor.authorSarkis, João José Freitaspt_BR
dc.contributor.authorStefanon, Ivanitapt_BR
dc.contributor.authorVassallo, Dalton Valentimpt_BR
dc.contributor.authorFürstenau, Cristina Ribaspt_BR
dc.date.accessioned2012-03-03T01:24:55Zpt_BR
dc.date.issued2011pt_BR
dc.identifier.issn0100-879Xpt_BR
dc.identifier.urihttp://hdl.handle.net/10183/37320pt_BR
dc.description.abstractGadolinium (Gd) blocks intra- and extracellular ATP hydrolysis. We determined whether Gd affects vascular reactivity to contractile responses to phenylephrine (PHE) by blocking aortic ectonucleoside triphosphate diphosphohydrolase (E-NTPDase). Wistar rats of both sexes (260-300 g, 23 females, 7 males) were used. Experiments were performed before and after incubation of aortic rings with 3 μM Gd. Concentration-response curves to PHE (0.1 nM to 0.1 mM) were obtained in the presence and absence of endothelium, after incubation with 100 μM L-NAME, 10 μM losartan, or 10 μM enalaprilat. Gd significantly increased the maximum response (control: 72.3 ± 3.5; Gd: 101.3 ± 6.4%) and sensitivity (control: 6.6 ± 0.1; Gd: 10.5 ± 2.8%) to PHE. To investigate the blockade of E-NTPDase activity by Gd, we added 1 mM ATP to the bath. ATP reduced smooth muscle tension and Gd increased its relaxing effect (control: -33.5 ± 4.1; Gd: -47.4 ± 4.1%). Endothelial damage abolished the effect of Gd on the contractile responses to PHE (control: 132.6 ± 8.6; Gd: 122.4 ± 7.1%). L-NAME + Gd in the presence of endothelium reduced PHE contractile responses (control/L-NAME: 151.1 ± 28.8; L-NAME + Gd: 67.9 ± 19% AUC). ATP hydrolysis was reduced after Gd administration, which led to ATP accumulation in the nutrient solution and reduced ADP concentration, while adenosine levels remained the same. Incubation with Gd plus losartan and enalaprilat eliminated the pressor effects of Gd. Gd increased vascular reactivity to PHE regardless of the reduction of E-NTPDase activity and adenosine production. Moreover, the increased reactivity to PHE promoted by Gd was endothelium-dependent, reducing NO bioavailability and involving an increased stimulation of angiotensin-converting enzyme and angiotensin II AT1 receptors.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofBrazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas. Ribeirão Preto, SP. Vol. 44, no. 5 (May 2011), p. 445-452pt_BR
dc.rightsOpen Accessen
dc.subjectHipertensãopt_BR
dc.subjectGadoliniumen
dc.subjectGadolíniopt_BR
dc.subjectE-NTPDaseen
dc.subjectAdenosineen
dc.subjectAdenosinapt_BR
dc.subjectAngiotensina IIpt_BR
dc.subjectAngiotensin IIen
dc.subjectAT1 receptoren
dc.titleGadolinium increases the vascular reactivity of rat aortic ringspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb000818611pt_BR
dc.type.originNacionalpt_BR


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