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Regulation of Renal Microcirculation in Ang II-Induced Hypertension

Regulation of Renal Microcirculation in Ang II-Induced Hypertension
血管紧张素II诱发高血压肾微循环的调节
批准号:
7249769
负责人:
Oscar A. Carretero
金额:
$24.74万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2007
资助国家:
美国
项目状态:
已结题
起止时间:
2007-09-01 至 2012-07-31
关键词:
AccountingAcidsAffectAldosteroneAmilorideAngiotensin-Converting Enzyme InhibitorsArachidonic AcidsArtsAutacoidsBathingBiostatistics CoreBloodBlood PressureBradykininBradykinin B2 ReceptorCardiovascular systemCationsCellsChelating AgentsCore FacilityCyclic AMPCyclic GMPCyclic GMP-Dependent Protein KinasesDataData AnalysesDevelopmentDiabetes MellitusDiffuseDilatation - actionDinoprostoneDistalDoctor of MedicineEicosanoidsEndocrineEndotheliumEpoprostenolEquilibriumExcretory functionFeedbackFiltrationFundingFutureGene DeletionGuanylate CyclaseHeart HypertrophyHormonesHypertensionIn VitroIonophoresKidneyKidney DiseasesKininogenaseKininsLimb structureLogisticsMacula densaMeasuresMediatingMediationMediator of activation proteinMicrocirculationModelingMorphologyMusMutant Strains MiceNG-Nitroarginine Methyl EsterNatriuresisNatriuretic FactorsNephronsNephrosclerosisNystatinOrganOryctolagus cuniculusPTGS2 genePathological DilatationPerfusionPhysiologicalPlayPrincipal InvestigatorProcessProductionProstaglandin AntagonistsProstaglandin E ReceptorProstaglandinsProstaglandins IProtein Kinase InhibitorsProteinsReceptor SignalingRegulationRenal functionReninReportingResearch DesignResearch PersonnelResistanceReverse Transcriptase Polymerase Chain ReactionRoleSignal TransductionSodiumSoluble Guanylate CyclaseStimulusSystemTechniquesTestingTherapeutic EffectThickThromboxanesTransgenic MiceValinomycinVascular resistanceVasoconstrictor AgentsVasodilationVasodilation disorderVasodilator AgentsWaterWorkabsorptionarterioleautocrinebasolateral membranechannel blockersepithelial Na+ channelglomerulosclerosisin vivoinhibitor/antagonistkidney vascular structurenephrinnovelparacrinepressureprogramsprotein kinase inhibitorreceptorresponsesensortempolvasoconstriction

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中文摘要
翻译
在血管紧张素II诱导的高血压中,压力尿钠排泄设定点转移到更高的压力,可能是由于 肾血管阻力和Na+重吸收增加。传入(Af-Art)和传出小动脉 (Ef-Art)占大多数肾血管阻力;它们控制GFR和管周压,从而影响肾血管阻力。 功能Af-Art抵抗力受有利于血管收缩的因素和那些 有利于血管扩张。我们的初步数据表明,增加Na+输送到连接小管, (CNT)会导致动脉扩张这种作用在这里被称为连接小管肾小球反馈(CTGF) 并且是有利于扩张的生理因素。研究CTGF的作用机制,同时避免其影响 我们建议使用我们开发的一种技术,该技术包括体外灌注一种 显微解剖的Af-Art和粘附的CNT。CNT不仅在Na+吸收和K+吸收中起重要作用, 分泌,而且还合成激肽释放酶,肾素,NO和类花生酸;然而,这些因素的作用, CTGF未知。我们建议测试C7 GF促进Af-Art扩张的一般假设 并因此拮抗血管收缩刺激物如Ang II和TGF。CTGF是由 花生四烯酸代谢产物。在血管紧张素II诱导的高血压期间,CTGF由于血管紧张素II诱导的高血压而增强。 联合作用的血管紧张素Ⅱ,O2'和醛固酮对Na* 转运;然而,在af-art这种刺激, 内皮源性收缩因子和CNT中NO的增加使其变钝。这一假设 将在以下测试中进行测试
英文摘要
In Ang ll-induced hypertension, the pressure natriuresis set point is shifted to a higher pressure, probably due to an increase in renal vascular resistance and Na+ reabsorption. The afferent (Af-Art) and efferent arterioles (Ef-Art) account for most renal vascular resistance; they control GFR and peritubular pressure, and thus renal function. Af-Art resistance is regulated by a balance between factors favoring vasoconstriction and those favoring vasodilatation. Our preliminary data indicate that increased Na+ delivery to the connecting tubule (CNT) causes Af-Art dilatation. This effect will here be called connecting tubule glomerular feedback (CTGF) and is a physiological factor favoring dilatation. To study the mechanism of CTGF while avoiding the influence of systemic factors, we propose to use a technique developed by us that consists of in vitro perfusion of a microdissected Af-Art and adherent CNT. The CNT not only plays an important role in Na+ absorption and K+ excretion but also synthesizes kallikrein, renin, NO and eicosanoids; however, the role of these factors in CTGF is unknown. We propose to test the general hypothesis that C7GF promotes dilatation of the Af-Art and thus antagonizes vasoconstrictor stimuli such as Ang II and TGF. CTGF is mediated by arachidonic acid metabolites. During Ang ll-induced hypertension, CTGF is enhanced due to the combined effects of Ang II, O2'andaldosterone on Na* transport; however, in theAf-Art this stimulation is bluntedby endothelium-derived constricting factors and by increased NO in the CNT. This hypothesis will be tested in the following
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