Soluble Guanylyl Cyclase (sgc) Degradation And Impairment Of Nitric Oxide-mediated Responses In Urethra From Obese Mice: Reversal By The Sgc Activator Bay 60-2770

dc.creatorAlexandre E.C.
dc.creatorLeiria L.O.
dc.creatorSilva F.H.
dc.creatorMendes-Silverio C.B.
dc.creatorCalmasini F.B.
dc.creatorDavel A.P.C.
dc.creatorMonica F.Z.
dc.creatorDe Nucci G.
dc.creatorAntunes E.
dc.date2014
dc.date2015-06-25T17:54:42Z
dc.date2015-11-26T14:36:12Z
dc.date2015-06-25T17:54:42Z
dc.date2015-11-26T14:36:12Z
dc.date.accessioned2018-03-28T21:39:50Z
dc.date.available2018-03-28T21:39:50Z
dc.identifier
dc.identifierJournal Of Pharmacology And Experimental Therapeutics. American Society For Pharmacology And Experimental Therapy, v. 349, n. 4, p. 2 - 9, 2014.
dc.identifier223565
dc.identifier10.1124/jpet.113.211029
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84896455248&partnerID=40&md5=fd2f8d3443d80bb747a5dcbc1ef47957
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/86741
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/86741
dc.identifier2-s2.0-84896455248
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1248639
dc.descriptionObesity has emerged as a major contributing risk factor for overactive bladder (OAB), but no study examined urethral smooth muscle (USM) dysfunction as a predisposing factor to obesity-induced OAB. This study investigated the USM relaxant machinery in obese mice and whether soluble guanylyl cyclase (sGC) activation with BAY 60-2770 [acid 4-({(4-carboxybutyl) [2-(5-fluoro-2-{[4- (trifluoromethyl) biphenyl-4-yl] methoxy} phenyl) ethyl] amino} methyl) benzoic] rescues the urethral reactivity through improvement of sGC-cGMP (cyclic guanosine monophosphate) signaling. Male C57BL/6 mice were fed for 12 weeks with a high-fat diet to induce obesity. Separate groups of animals were treated with BAY 60-2770 (1 mg/kg per day for 2 weeks). Functional assays and measurements of cGMP, reactive-oxygen species (ROS), and sGC protein expression in USM were determined. USM relaxations induced by NO (acidified sodium nitrite), NO donors (S-nitrosoglutathione and glyceryl trinitrate), and BAY 41-2272 [5-cyclopropyl-2-[1-(2-fluoro-benzyl)-1H-pyrazolo[3,4-b] pyridin-3-yl]- pyrimidin-4-ylamine] (sGC stimulator) were markedly reduced in obese compared with lean mice. In contrast, USM relaxations induced by BAY 60-2770 (sGC activator) were 43% greater in obese mice (P < 0.05), which was accompanied by increases in cGMP levels. Oxidation of sGC with ODQ [1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one] (10 μM) potentiated BAY 60-2770-induced USM responses in the lean group. Long-term oral BAY 60-2770 administration fully prevented the impairment of USM relaxations in obese mice. Reactive-oxygen species (ROS) production was enhanced, but protein expression of β1 second guanylate cyclase subunit was reduced in USMfrom obesemice, both of which were restored by BAY 60-2770 treatment. In conclusion, impaired USM relaxation in obese mice is associated with ROS generation and down-regulation of sGC-cGMP signaling. Prevention of sGC degradation by BAY 60-2770 ameliorates the impairment of urethral relaxations in obese mice. Copyright © 2014 by The American Society for Pharmacology and Experimental Therapeutics.
dc.description349
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dc.description2
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dc.languageen
dc.publisherAmerican Society for Pharmacology and Experimental Therapy
dc.relationJournal of Pharmacology and Experimental Therapeutics
dc.rightsfechado
dc.sourceScopus
dc.titleSoluble Guanylyl Cyclase (sgc) Degradation And Impairment Of Nitric Oxide-mediated Responses In Urethra From Obese Mice: Reversal By The Sgc Activator Bay 60-2770
dc.typeArtículos de revistas


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