Glybenclamide regulate ERK1/2 signal pathway during hypoxia hypercapnia pulmonary vasoconstriction in rats / 中国应用生理学杂志
Chinese Journal of Applied Physiology
; (6): 110-114, 2014.
Article
em Zh
| WPRIM
| ID: wpr-236372
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WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the role and significance of ATP-sensitive K+ channels in the pathological process of hypoxia hypercapnia-induced pulmonary vasoconstriction (HHPV) and the relationship with ERK1/2 signal pathway in rats.</p><p><b>METHODS</b>We made the third pulmonary artery rings of SD rats, used the model of pulmonary artery rings perfusion in vitro. Under acute hypoxia hypercapnia condition, and observed the effects of the three stages of HHPV incubated by glybenclamide(Gly) and the combined application of Gly and U0126. At the same time, the values of rings' tension changes were recorded via the method of hypoxia hypercapnia conditions reactivity.</p><p><b>RESULTS</b>Under the normoxia condition, the values of the third pulmonary artery rings tension were relatively stable, but under the hypoxia hypercapnia condition, we observed a biphasic pulmonary artery contractile response compared with N group (P < 0.05, P < 0.01). When the third pulmonary artery rings incubated by Gly, it's phase II persistent vasoconstriction was enhanced compared with the H group (P < 0.05, P < 0.01), and the phase I vasoconstriction was also heightened. Moreover, under the hypoxia hypercapnia condition, U0126 could significantly relieve the phase II persistent vasoconstriction compared with HD group (P < 0.05, P < 0.01) induced by Gly, but the phase I acute vasoconstriction and the phase I vasodilation had no changes (P > 0.05).</p><p><b>CONCLUSION</b>Gly may mediate HHPV via activating ERK1/2 signal transduction pathway.</p>
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Assunto principal:
Farmacologia
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Fisiologia
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Artéria Pulmonar
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Vasoconstrição
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Técnicas In Vitro
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Glibureto
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Ratos Sprague-Dawley
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Sistema de Sinalização das MAP Quinases
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Hipercapnia
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Hipóxia
Limite:
Animals
Idioma:
Zh
Revista:
Chinese Journal of Applied Physiology
Ano de publicação:
2014
Tipo de documento:
Article