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
基本信息
- 批准号:7249769
- 负责人:
- 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
- 起止时间:2007-09-01 至 2012-07-31
- 项目状态:已结题
- 来源:
- 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
项目摘要
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
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Na+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,钠离子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Na~+吸收和K~+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
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Oscar A. Carretero其他文献
Ren-2 Gene Salt Hypertensive Mice Lacking − Antagonist in Deoxycorticosterone Acetate Effects of Angiotensin-converting Enzyme Inhibitor and Angiotensin Type 1 Receptor
Ren-2基因盐高血压小鼠缺乏-醋酸脱氧皮质酮拮抗剂对血管紧张素转换酶抑制剂和血管紧张素1型受体的影响
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
Hongmei Peng;Oscar A. Carretero;M. Alfie;Julie A. Masura;N. Rhaleb - 通讯作者:
N. Rhaleb
Cross-talk between arterioles and tubules in the kidney
- DOI:
10.1007/s00467-008-0852-8 - 发表时间:
2009-01-01 - 期刊:
- 影响因子:2.600
- 作者:
YiLin Ren;Jeffrey L. Garvin;Ruisheng Liu;Oscar A. Carretero - 通讯作者:
Oscar A. Carretero
Effects of propranolol on the development of renovascular hypertension in the rat
- DOI:
10.1016/s0002-8703(77)80347-5 - 发表时间:
1977-07-01 - 期刊:
- 影响因子:
- 作者:
Andreas P. Niarchos;Om P. Gulati;Oscar A. Carretero - 通讯作者:
Oscar A. Carretero
Urinary kallikrein and plasma renin during the reversal of renovascular hypertension in rats.
大鼠肾血管性高血压逆转过程中的尿激肽释放酶和血浆肾素。
- DOI:
- 发表时间:
1976 - 期刊:
- 影响因子:0
- 作者:
O. P. Gulati;Oscar A. Carretero;T. Morino;N. B. Oza - 通讯作者:
N. B. Oza
Kinins mediate the antiproliferative effect of ramipril in rat carotid artery.
激肽介导雷米普利在大鼠颈动脉中的抗增殖作用。
- DOI:
- 发表时间:
1992 - 期刊:
- 影响因子:0
- 作者:
R. Farhy;Khang;Oscar A. Carretero;A. Scicli - 通讯作者:
A. Scicli
Oscar A. Carretero的其他文献
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{{ truncateString('Oscar A. Carretero', 18)}}的其他基金
Tubuloglomerular Feedback Regulation by Carbon Monoxide
一氧化碳的肾小球反馈调节
- 批准号:
8376983 - 财政年份:2012
- 资助金额:
$ 24.74万 - 项目类别:
Regulation of the Renal Microcirculation by the Connecting Tubule
连接小管对肾脏微循环的调节
- 批准号:
7356857 - 财政年份:2008
- 资助金额:
$ 24.74万 - 项目类别:
Regulation of the Renal Microcirculation by the Connecting Tubule
连接小管对肾脏微循环的调节
- 批准号:
8034726 - 财政年份:2008
- 资助金额:
$ 24.74万 - 项目类别:
Regulation of the Renal Microcirculation by the Connecting Tubule
连接小管对肾脏微循环的调节
- 批准号:
7766928 - 财政年份:2008
- 资助金额:
$ 24.74万 - 项目类别:
Regulation of the Renal Microcirculation by the Connecting Tubule
连接小管对肾脏微循环的调节
- 批准号:
7580940 - 财政年份:2008
- 资助金额:
$ 24.74万 - 项目类别:
Ang II-Induced Hypertension: Role of Ac-SDKP in End Organ Damage
Ang II 诱发的高血压:Ac-SDKP 在终末器官损伤中的作用
- 批准号:
7249766 - 财政年份:2007
- 资助金额:
$ 24.74万 - 项目类别:
AUTOCRINE/PARACRINE REGULATION OF RENAL MICROCIRCULATION
肾微循环的自分泌/旁分泌调节
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6649479 - 财政年份:2002
- 资助金额:
$ 24.74万 - 项目类别:
Ac-SDKP in target organ damage in hypertension
Ac-SDKP 在高血压靶器官损伤中的作用
- 批准号:
6649484 - 财政年份:2002
- 资助金额:
$ 24.74万 - 项目类别:
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