Regulation of Renal Microcirculation in Ang II-Induced Hypertension
Regulation of Renal Microcirculation in Ang II-Induced Hypertension
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
中文摘要
在血管紧张性高血压中,压力钠尿设定点向更高的压力移动,这可能是由于
增加肾血管阻力和钠重吸收。传入(Af-Art)和传出小动脉
(EF-ART)解释了大多数肾血管阻力;它们控制GFR和管周压力,从而控制肾脏
功能。房颤-ART抵抗是由有利于血管收缩的因素和那些
有利于血管扩张的。我们的初步数据显示,钠向连接小管的输送增加
(CNT)导致Af-Art扩张。这种效应在这里被称为连接小管肾小球反馈(CTGF)。
是一种有利于扩张的生理因素。在避免影响的同时研究CTGF的作用机理
我们建议使用我们开发的一种技术,该技术包括体外灌流一种
显微解剖Af-Art和贴壁CNT。碳纳米管不仅在钠和钾的吸收中起重要作用
排泄还合成激肽释放酶、肾素、一氧化氮和二十烷类化合物;然而,这些因素在
CTGF尚不清楚。我们建议检验C7GF促进房颤-ART扩张的普遍假设
从而拮抗血管收缩刺激,如血管紧张素II和转化生长因子。CTGF通过以下方式进行调节
花生四烯酸代谢物。在AngⅡ诱导性高血压期间,CTGF由于
Ang II、O2‘和醛固酮联合作用对Na~*转运的影响
被内皮衍生的收缩因子和CNT中增加的NO所钝化。这一假设
将在以下方面进行测试
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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批准号:7356857
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Regulation of the Renal Microcirculation by the Connecting Tubule
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Regulation of the Renal Microcirculation by the Connecting Tubule
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批准号:7580940
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资助金额:$32.63万
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Administrative Core
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批准号:7249774
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依托单位:
AUTOCRINE/PARACRINE REGULATION OF RENAL MICROCIRCULATION
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批准号:6649479
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项目类别:
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资助金额:$7.35万
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Ac-SDKP in target organ damage in hypertension
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批准号:6649484
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资助金额:$7.35万
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财政年份:2002
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PARACRINE REGULATION OF THE RENAL MICROCIRCULATION
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批准号:6495723
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依托单位:
KININS--CARDIOPROTECTIVE EFFECTS
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KININS--CARDIOPROTECTIVE EFFECTS
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资助金额:$19.21万
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