Role of ATP-sensitive potassium channels in normal and hypertension-associated pregnancy in rats

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dc.contributor.authorLima, R.
dc.contributor.authorTardim, J. C. B. M.
dc.contributor.authorBarros, M. E.
dc.contributor.authorBoim, M. A.
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:41:27Z
dc.date.available2016-01-24T12:41:27Z
dc.date.issued2006-09-01
dc.description.abstractActivation of vascular ATP-sensitive K+ (K-ATP) channels has been implicated in vasodilator responses to pregnancy.The effect of glibenclamide, a K-ATP channel inhibitor, on systolic blood pressure (SBP) and renal function was evaluated in pregnant and non-pregnant spontaneously hypertensive rats, as well as in normotensive and hypertensive Wistar rats that had been made hypertensive by simultaneous treatment with N-G-nitro-(L)-arginine methyl ester (0.4 mg/mL) and indomethacin (2 mg/kg, i.p.) from Day 1 of gestation. Pregnant animals received 10 mg/kg glibenclamide for 12 days starting at Day 7. in addition, the mRNA levels of the vascular K-ATP channel (Kir6.2) were estimated in aorta and kidney using real-time reverse transcription-polymerase chain reaction on Day 19 of pregnancy.The decreased SBP observed in pregnant Wistar rats was paralleled by an increase in Kir6.2 mRNA levels. Glibenclamide blunted systemic vasodilation and reduced the mRNA expression of Kir6.2. There was no pregnancy induced vasodilation and no change in Kir6.2 mRNA expression in SHR. Glibenclamide had no effect on pregnant SHR. Hypertensive Wistar rats exhibited high SBP, followed by increased Kir6.2 mRNA levels. the effects of glibenclamide were not evaluated in this group because glibenclamide induced intense vaginal bleeding.The results of the present study suggest that K-ATP channels may be involved in pregnancy induced vasodilation during normotensive pregnancy, but not in pregnant SHR. Glibenclamide may have an abortive effect if administered during the early phases of gestation or in association with nitric oxide and prostaglandin inhibitors.en
dc.description.affiliationUniversidade Federal de São Paulo, Div Renal, BR-04023900 São Paulo, SP, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Div Renal, BR-04023900 São Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.format.extent780-786
dc.identifierhttp://dx.doi.org/10.1111/j.1440-1681.2006.04438.x
dc.identifier.citationClinical and Experimental Pharmacology and Physiology. Oxford: Blackwell Publishing, v. 33, n. 9, p. 780-786, 2006.
dc.identifier.doi10.1111/j.1440-1681.2006.04438.x
dc.identifier.issn0305-1870
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29146
dc.identifier.wosWOS:000239659300003
dc.language.isoeng
dc.publisherBlackwell Publishing
dc.relation.ispartofClinical and Experimental Pharmacology and Physiology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjecthypertensionen
dc.subjectK-ATP channelsen
dc.subjectnitric oxideen
dc.subjectpregnancyen
dc.subjectspontaneously hypertensive ratsen
dc.titleRole of ATP-sensitive potassium channels in normal and hypertension-associated pregnancy in ratsen
dc.typeinfo:eu-repo/semantics/article
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