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Gadolinium increases the vascular reactivity of rat aortic rings

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Gadolinium increases the vascular reactivity of rat aortic rings

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Título Gadolinium increases the vascular reactivity of rat aortic rings
Autor Angeli, Jully Kely
Ramos, Denise Barbosa
Casali, Emerson Andre
Souza, Diogo Onofre Gomes de
Sarkis, João José Freitas
Stefanon, Ivanita
Vassallo, Dalton Valentim
Fürstenau, Cristina Ribas
Abstract Gadolinium (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.
Contido em Brazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas. São Paulo. Vol. 44, no. 5 (May 2011), p. 445-452
Assunto Adenosina
Angiotensina II
Gadolínio
Hipertensão
[en] Adenosine
[en] Angiotensin II
[en] AT1 receptor
[en] E-NTPDase
[en] Gadolinium
Origem Nacional
Tipo Artigo de periódico
URI http://hdl.handle.net/10183/37320
Arquivos Descrição Formato
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