2014
Postmenopausal Hypertension and Sodium Sensitivity
Kim J, Kim T, Lee H, Lee S, Wang T. Postmenopausal Hypertension and Sodium Sensitivity. Journal Of Menopausal Medicine 2014, 20: 1-6. PMID: 25371885, PMCID: PMC4217569, DOI: 10.6118/jmm.2014.20.1.1.Peer-Reviewed Original ResearchReduced systolic BPBlood pressureSystolic BPSex hormonesDevelopment of postmenopausal hypertensionOral hormone replacement therapyEffect of salt intakeElevation of systolic BPAngiotensin type 2 receptorPrevalence of salt sensitivityAnti-aldosterone activityHormone replacement therapyLack of estrogenWomen to levelsIncidence rate of hypertensionLow-salt dietPost-menopausal womenType 2 receptorFemale sex hormonesRegulation of arterial pressureRenal regulatory mechanismsNitric oxideSalt sensitivityStimulate nitric oxideRates of hypertension
2012
Identification of renin signaling as a blood pressure modifying mechanism in soluble guanylate cyclase α1-deficient mice
Buys E, Raher M, Kirby A, Mohd S, Baron D, Hayton S, Tainsh L, Sips P, Rauwerdink K, Tainsh R, Shakartzi H, Stevens C, Decaluwé K, da Gloria Rodrigues-Machado M, Malhotra R, Van de Voorde J, Wang T, Brouckaert P, Daly M, Bloch K. Identification of renin signaling as a blood pressure modifying mechanism in soluble guanylate cyclase α1-deficient mice. Nitric Oxide 2012, 27: s25-s26. DOI: 10.1016/j.niox.2012.04.093.Peer-Reviewed Original ResearchRenin-angiotensin-aldosterone systemQuantitative trait lociRenin-angiotensin-aldosterone system signalingPlasma angiotensin II levelsEtiology of human hypertensionPlasma aldosterone levelsGlomerular filtration rateNitric oxideNO-cGMP signalingAngiotensin II levelsEndothelium-dependent vasorelaxationImpaired NO-cGMP signalingBlood urea nitrogenSubunit of soluble guanylate cyclaseAssociated with increased activitySoluble guanylate cyclaseImproving endothelium-dependent vasorelaxationRegulating blood pressureAldosterone levelsB6 miceMale F2 offspringNO-cGMPRenal functionUrinary volumeEssential hypertensionGenetic modifiers of hypertension in soluble guanylate cyclase α1–deficient mice
Buys E, Raher M, Kirby A, Mohd S, Baron D, Hayton S, Tainsh L, Sips P, Rauwerdink K, Yan Q, Tainsh R, Shakartzi H, Stevens C, Decaluwé K, da Gloria Rodrigues-Machado M, Malhotra R, Van de Voorde J, Wang T, Brouckaert P, Daly M, Bloch K. Genetic modifiers of hypertension in soluble guanylate cyclase α1–deficient mice. Journal Of Clinical Investigation 2012, 122: 2316-2325. PMID: 22565307, PMCID: PMC3366402, DOI: 10.1172/jci60119.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCyclic GMPEndothelium, VascularFemaleGenetic LinkageGenome, HumanGuanylate CyclaseHumansHypertensionMaleMiceMice, KnockoutQuantitative Trait LociRatsReceptors, Cytoplasmic and NuclearReninRenin-Angiotensin SystemSecond Messenger SystemsSoluble Guanylyl CyclaseSpecies SpecificityVasodilationConceptsRenin-angiotensin-aldosterone systemRenin-angiotensin-aldosterone system inhibitionRelaxation of vascular smooth muscleVascular smooth muscleInducing relaxation of vascular smooth muscleNitric oxideEndothelium-dependent vasorelaxationSubunit of soluble guanylate cyclaseSoluble guanylate cyclaseImproving endothelium-dependent vasorelaxationSmooth muscleQuantitative trait lociArterial pressureMale miceMouse strainsNO/cGMP signalingInduced relaxationAssociated with increased activityHypertensionGuanylate cyclaseBlood flowMiceGenetic modifiersReceptor componentsGenetic factors
2002
Use of transgenic animals to study renal acid-base transport.
Wang T, Giebisch G, Aronson PS. Use of transgenic animals to study renal acid-base transport. Journal Of Nephrology 2002, 15 Suppl 5: s151-60. PMID: 12027214.Commentaries, Editorials and LettersConceptsAcid-base transportSpecific transporter isoformsSuch knockout miceRenal acid-base transportRenal acid-base homeostasisTransgenic miceTransporter isoformsPump subunitsTransgenic animalsKnockout micePhysiological roleATPase isoformsTransport deficiencyMolecular levelAcid-base homeostasisIsoformsAdaptive mechanismsCarbonic anhydraseCompensatory-adaptive mechanismsUseful experimental modelTransportersRegulatory mediatorsNHE isoformsNitric oxideExperimental model
1997
Nitric oxide regulates HCO3- and Na+ transport by a cGMP-mediated mechanism in the kidney proximal tubule
Wang T. Nitric oxide regulates HCO3- and Na+ transport by a cGMP-mediated mechanism in the kidney proximal tubule. American Journal Of Physiology 1997, 272: f242-f248. PMID: 9124402, DOI: 10.1152/ajprenal.1997.272.2.f242.Peer-Reviewed Original ResearchConceptsKidney proximal tubulesS-nitroso-N-acetylpenicillamineSodium nitroprussideProximal tubulesL-NAMEGuanylate cyclase inhibitor methyleneN(G)-nitro-L-arginine methyl esterBlood pressureNitric oxideNa+ transportStimulatory effect of sodium nitroprussideN(G)-nitro-L-arginineNitric oxide synthase inhibitorCGMP-mediated mechanismAddition of L-NAMEIncreased urine flow rateGlomerular filtration rateEffects of sodium nitroprussideMean blood pressureUrine flow rateEffects of nitric oxideRenal excretion of NaExcretion of NaRenal hemodynamicsEffects of NO