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dc.contributor.authorWalsh, Sarah K
dc.contributor.authorEnglish, Fred A
dc.contributor.authorJohns, Edward J
dc.contributor.authorKenny, Louise C
dc.date.accessioned2012-01-31T16:42:27Z
dc.date.available2012-01-31T16:42:27Z
dc.date.issued2012-01-31T16:42:27Z
dc.identifier.citationHypertension. 2009 Aug;54(2):345-51. Epub 2009 Jun 29.en_GB
dc.identifier.issn1524-4563 (Electronic)en_GB
dc.identifier.issn0194-911X (Linking)en_GB
dc.identifier.pmid19564546en_GB
dc.identifier.doi10.1161/HYPERTENSIONAHA.109.132191en_GB
dc.identifier.urihttp://hdl.handle.net/10147/206209
dc.description.abstractPreeclampsia is associated with widespread maternal vascular dysfunction, which is thought to be mediated by circulating factor(s). The aim of the study was to characterize vascular function in the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia and to investigate the role of plasma factors in mediating any observed changes in vascular reactivity. Mean arterial blood pressure and vascular function were measured in RUPP and control rats. Mesenteric vessels from both virgin and pregnant rats were exposed for 1 hour or overnight to plasma from both RUPP and control rats and their vascular function assessed. RUPP rats were characterized by severe hypertension, restricted fetal growth, and reduced placental weight (P<0.001). Vasorelaxation was impaired in resistance vessels from RUPP compared with control rats (acetylcholine: R(max) 70+/-3 versus 92+/-1 [NP] and 93+/-3% [sham], P<0.01; bradykinin: 40+/-2 versus 62+/-2 [NP] and 59+/-4% [sham], P<0.001). Incubation of vessels from pregnant (but not virgin) animals with RUPP plasma overnight resulted in an attenuation of vasorelaxant responses (acetylcholine: 63+/-7 versus 86+/-2%, P<0.05; bradykinin: 35+/-5 versus 55+/-6%, P<0.001). The residual relaxant response in RUPP plasma-treated vessels was not further attenuated after treatment with N(omega)-nitro-l-arginine methyl ester (acetylcholine: 57+/-7 versus 63+/-7%, ns; bradykinin: 37+/-5 versus 35+/-5%, ns). The RUPP rat model is characterized by an impaired response to vasodilators which may be attributable to one or more circulating factors. This plasma-mediated endothelial dysfunction appears to be a pregnancy-dependent effect. Furthermore, nitric oxide-mediated vasorelaxation appears to be absent in RUPP plasma-treated vessels.
dc.language.isoengen_GB
dc.subject.meshAnalysis of Varianceen_GB
dc.subject.meshAnimalsen_GB
dc.subject.meshBlood Pressure Determinationen_GB
dc.subject.meshDisease Models, Animalen_GB
dc.subject.meshEndothelium, Vascular/physiologyen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshMicrocirculation/drug effects/*physiologyen_GB
dc.subject.meshNG-Nitroarginine Methyl Ester/*pharmacologyen_GB
dc.subject.meshNitric Oxide/*metabolismen_GB
dc.subject.meshPerfusion/methodsen_GB
dc.subject.meshPlacenta/blood supplyen_GB
dc.subject.meshPre-Eclampsia/*physiopathologyen_GB
dc.subject.meshPregnancyen_GB
dc.subject.meshPressureen_GB
dc.subject.meshProbabilityen_GB
dc.subject.meshRandom Allocationen_GB
dc.subject.meshRatsen_GB
dc.subject.meshRats, Sprague-Dawleyen_GB
dc.subject.meshRisk Factorsen_GB
dc.subject.meshUterus/*blood supplyen_GB
dc.subject.meshVasoconstriction/drug effects/physiologyen_GB
dc.subject.meshVasodilation/drug effects/physiologyen_GB
dc.titlePlasma-mediated vascular dysfunction in the reduced uterine perfusion pressure model of preeclampsia: a microvascular characterization.en_GB
dc.contributor.departmentAnu Research Centre, Department of Obstetrics and Gynaecology, University College, Cork, Cork University Maternity Hospital, Wilton, Cork, Ireland. S.Walsh@ucc.ieen_GB
dc.identifier.journalHypertensionen_GB
dc.description.provinceMunster
html.description.abstractPreeclampsia is associated with widespread maternal vascular dysfunction, which is thought to be mediated by circulating factor(s). The aim of the study was to characterize vascular function in the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia and to investigate the role of plasma factors in mediating any observed changes in vascular reactivity. Mean arterial blood pressure and vascular function were measured in RUPP and control rats. Mesenteric vessels from both virgin and pregnant rats were exposed for 1 hour or overnight to plasma from both RUPP and control rats and their vascular function assessed. RUPP rats were characterized by severe hypertension, restricted fetal growth, and reduced placental weight (P<0.001). Vasorelaxation was impaired in resistance vessels from RUPP compared with control rats (acetylcholine: R(max) 70+/-3 versus 92+/-1 [NP] and 93+/-3% [sham], P<0.01; bradykinin: 40+/-2 versus 62+/-2 [NP] and 59+/-4% [sham], P<0.001). Incubation of vessels from pregnant (but not virgin) animals with RUPP plasma overnight resulted in an attenuation of vasorelaxant responses (acetylcholine: 63+/-7 versus 86+/-2%, P<0.05; bradykinin: 35+/-5 versus 55+/-6%, P<0.001). The residual relaxant response in RUPP plasma-treated vessels was not further attenuated after treatment with N(omega)-nitro-l-arginine methyl ester (acetylcholine: 57+/-7 versus 63+/-7%, ns; bradykinin: 37+/-5 versus 35+/-5%, ns). The RUPP rat model is characterized by an impaired response to vasodilators which may be attributable to one or more circulating factors. This plasma-mediated endothelial dysfunction appears to be a pregnancy-dependent effect. Furthermore, nitric oxide-mediated vasorelaxation appears to be absent in RUPP plasma-treated vessels.


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