| dc.creator | Teixeira C.E. | |
| dc.creator | Priviero F.B.M. | |
| dc.creator | Todd Jr. J. | |
| dc.creator | Webb R.C. | |
| dc.date | 2006 | |
| dc.date | 2015-06-30T18:01:54Z | |
| dc.date | 2015-11-26T14:16:03Z | |
| dc.date | 2015-06-30T18:01:54Z | |
| dc.date | 2015-11-26T14:16:03Z | |
| dc.date.accessioned | 2018-03-28T21:17:01Z | |
| dc.date.available | 2018-03-28T21:17:01Z | |
| dc.identifier | | |
| dc.identifier | Hypertension. , v. 47, n. 3 II, p. 596 - 602, 2006. | |
| dc.identifier | 0194911X | |
| dc.identifier | 10.1161/01.HYP.0000199914.36936.1b | |
| dc.identifier | http://www.scopus.com/inward/record.url?eid=2-s2.0-33644981623&partnerID=40&md5=74d8e55fca852585a596e9b2cddf2d1b | |
| dc.identifier | http://www.repositorio.unicamp.br/handle/REPOSIP/102745 | |
| dc.identifier | http://repositorio.unicamp.br/jspui/handle/REPOSIP/102745 | |
| dc.identifier | 2-s2.0-33644981623 | |
| dc.identifier.uri | http://repositorioslatinoamericanos.uchile.cl/handle/2250/1242960 | |
| dc.description | Decreases in intrinsic NO cause cerebral vasospasms because of the dysregulation of cGMP formation by NO-mediated pathways. Because 5-cyclopropyl-2-{1-(2-fluorobenzyl)-1H-pyrazolo[3,4-b]pyridin-3-yl} pyrimidin-4-ylamine (BAY 41-2272) is a potent soluble guanylyl cyclase (sGC) stimulator in an NO-independent manner, this study aimed to investigate the mechanisms underlying the relaxant effects of BAY 41-2272 in the rat basilar artery. BAY 41-2272 (0.0001 to 1 μmol/L) induced relaxations in a concentration-dependent manner, with pEC50 values of 8.13±0.03 and 7.63±0.05 in intact and denuded rings, respectively. The sGC inhibitor 1H-[1,2,4] oxadiazolo [4,3,-a]quinoxalin-1-one (ODQ) markedly displaced the curve for BAY 41-2272 to the right in intact or denuded rings (≈10-fold). The NO synthesis inhibitor NG-nitro-L-arginine methyl ester caused a rightward shift in the curve for BAY 41-2272 (4-fold), whereas the phosphodiesterase type 5 inhibitor sildenafil enhanced BAY 41-2272-induced relaxations (3- to 4-fold). The Na+-K+-ATPase inhibitor ouabain caused 3-fold rightward shifts in the curves for BAY 41-2272. Ca 2+-induced contractions in K+ depolarized rings were significantly attenuated by BAY 41-2272 in an ODQ-insensitive manner. The NO donor glyceryl trinitrate and BAY 41-2272 caused rightward shifts in the contractile responses to serotonin. Their coincubation caused a synergistic inhibition of serotonin-induced contractions. BAY 41-2272 and glyceryl trinitrate increased cGMP levels (but not cAMP) by 10-fold and 4-fold above baseline, respectively, in an ODQ-sensitive manner. cGMP levels increased by 50-fold after coincubation. BAY 41-2272 potently relaxes the rat basilar artery in a synergistic fashion with NO. Targeting the sGC with selective activators, such as BAY 41-2272, may represent a new therapy to treat cerebrovascular disease. © 2006 American Heart Association, Inc. | |
| dc.description | 47 | |
| dc.description | 3 II | |
| dc.description | 596 | |
| dc.description | 602 | |
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| dc.language | en | |
| dc.publisher | | |
| dc.relation | Hypertension | |
| dc.rights | fechado | |
| dc.source | Scopus | |
| dc.title | Vasorelaxing Effect Of Bay 41-2272 In Rat Basilar Artery: Involvement Of Cgmp-dependent And Independent Mechanisms | |
| dc.type | Actas de congresos | |
