2023
Comprehensive Characterization of Coagulation Parameters in Venous Malformations
Restrepo V, Pine A, Butt A, Chang E, Bar N, Baluha A, Brooks A, Chirico G, Curran J, Dumont A, Obura-Wilkes P, Rinder H, Tormey C, Nassiri N, Lee A, Prozora S. Comprehensive Characterization of Coagulation Parameters in Venous Malformations. Blood 2023, 142: 27. DOI: 10.1182/blood-2023-190609.Peer-Reviewed Original ResearchHigher thrombin-antithrombin complexesNormal D-dimerThrombin-antithrombin complexPlasminogen activator inhibitor-1Localized intravascular coagulopathyInternational normalized ratioD-dimerVenous malformationsCoagulation parametersPartial thromboplastin timeCoagulation testsFactor VIIIVWF activityChart reviewMost patientsHematology clinicProthrombin timeTissue involvementVWF antigenVon Willebrand factor antigenHigher TAT levelsMultiple coagulation parametersBaseline patient characteristicsRetrospective chart reviewCoagulation test resultsAssociation of SNPs in the PAI1 Gene with Disease Recurrence and Clinical Outcome in Bladder Cancer
Murakami K, Furuya H, Hokutan K, Goodison S, Pagano I, Chen R, Shen C, Chan M, Ng C, Kobayashi T, Ogawa O, Miyake M, Thornquist M, Shimizu Y, Hayashi K, Wang Z, Yu H, Rosser C. Association of SNPs in the PAI1 Gene with Disease Recurrence and Clinical Outcome in Bladder Cancer. International Journal Of Molecular Sciences 2023, 24: 4943. PMID: 36902377, PMCID: PMC10003630, DOI: 10.3390/ijms24054943.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Bladder cancerSingle nucleotide polymorphismsMutational statusWorse recurrence-free survivalUntranslated region (UTR) single nucleotide polymorphismRecurrence-free survivalBladder cancer developmentHuman bladder tumorsAssociation of SNPsCommon cancer typesActivator inhibitor-1Anti-apoptotic effectsOverall survivalDisease recurrenceClinical outcomesOverall incidenceBladder tumorsCaucasian patientsIndependent cohortCancer typesCancer developmentCancerInhibitor-1Cellular proliferation
2022
Comparative effects of weight loss and incretin‐based therapies on vascular endothelial function, fibrinolysis and inflammation in individuals with obesity and prediabetes: A randomized controlled trial
Mashayekhi M, Beckman JA, Nian H, Garner EM, Mayfield D, Devin JK, Koethe JR, Brown JD, Cahill KN, Yu C, Silver H, Niswender K, Luther JM, Brown NJ. Comparative effects of weight loss and incretin‐based therapies on vascular endothelial function, fibrinolysis and inflammation in individuals with obesity and prediabetes: A randomized controlled trial. Diabetes Obesity And Metabolism 2022, 25: 570-580. PMID: 36306151, PMCID: PMC10306232, DOI: 10.1111/dom.14903.Peer-Reviewed Original ResearchConceptsFlow-mediated vasodilationPlasminogen activator inhibitor-1Vascular endothelial functionEndothelial functionInsulin resistanceWeight lossGlucagon-like peptide-1 receptor agonistsBaseline flow-mediated vasodilationDipeptidyl peptidase-4 inhibitor sitagliptinGLP-1R agonist liraglutideWeight loss-independent mechanismsPeptide-1 receptor agonistsBeneficial effectsEndothelial vasodilator functionGreater endothelial dysfunctionIncretin-based therapiesNormal endothelial functionChemoattractant protein-1Chemokine MCP-1Significant weight lossActivator inhibitor-1Effect of treatmentVasodilator functionUrine albuminEndothelial dysfunctionThe obesity paradox: Retinopathy, obesity, and circulating risk markers in youth with type 2 diabetes in the TODAY Study
Levitsky LL, Drews KL, Haymond M, Glubitosi-Klug RA, Katz L, Mititelu M, Tamborlane W, Tryggestad JB, Weinstock RS, Group T. The obesity paradox: Retinopathy, obesity, and circulating risk markers in youth with type 2 diabetes in the TODAY Study. Journal Of Diabetes And Its Complications 2022, 36: 108259. PMID: 36150365, DOI: 10.1016/j.jdiacomp.2022.108259.Peer-Reviewed Original ResearchConceptsNon-proliferative diabetic retinopathyType 2 diabetesHigh-sensitivity C-reactive proteinObesity paradoxInflammatory biomarkersHDL cholesterolLDL cholesterolInsulin-like growth factor binding protein 1Sensitivity C-reactive proteinGrowth factor binding protein 1Today StudyPresence of retinopathyRelationship of obesityC-reactive proteinPlasminogen activator inhibitor-1Tumor necrosis factor receptor 1Digital fundus photographsNecrosis factor receptor 1Activator inhibitor-1Factor receptor 1Higher BMIObese participantsRisk markersDiabetic retinopathyInterleukin-6
2017
Genetic Effects on the Correlation Structure of CVD Risk Factors Exome-Wide Data From a Ghanaian Population
Kodaman N, Sobota RS, Asselbergs FW, Oetjens MT, Moore JH, Brown NJ, Aldrich MC, Williams SM. Genetic Effects on the Correlation Structure of CVD Risk Factors Exome-Wide Data From a Ghanaian Population. Global Heart 2017, 12: 133-140. PMID: 28408189, PMCID: PMC5642993, DOI: 10.1016/j.gheart.2017.01.013.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1CVD risk factorsRisk factorsCardiovascular disease risk factorsDisease risk factorsHigh blood pressureActivator inhibitor-1Dissolution of thrombusArterial pressureBlood pressureMyocardial infarctionPlasma concentrationsStudy participantsGhanaian populationInhibitor-1Significant heterogeneityHeterogeneity of correlationAfrican AmericansGenetic variantsGenetic association studiesDirect role
2016
Plasminogen Activator Inhibitor‐1 and Diagnosis of the Metabolic Syndrome in a West African Population
Kodaman N, Aldrich MC, Sobota R, Asselbergs FW, Brown NJ, Moore JH, Williams SM. Plasminogen Activator Inhibitor‐1 and Diagnosis of the Metabolic Syndrome in a West African Population. Journal Of The American Heart Association 2016, 5: e003867. PMID: 27697752, PMCID: PMC5121488, DOI: 10.1161/jaha.116.003867.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAntihypertensive AgentsBlood GlucoseBlood PressureBody Mass IndexCholesterol, HDLCross-Sectional StudiesDiabetes MellitusFastingFemaleGhanaHumansHypertensionHypoglycemic AgentsMaleMetabolic SyndromeMiddle AgedPlasminogen Activator Inhibitor 1PrevalenceRural PopulationTriglyceridesUrban PopulationYoung AdultConceptsPlasminogen activator inhibitor-1Activator inhibitor-1Metabolic syndromeRisk factorsDiagnostic criteriaLow high-density lipoproteinInhibitor-1Relevance of MetSAge-standardized prevalenceConventional risk factorsCardiovascular disease riskBody mass indexMetS diagnostic criteriaPAI-1 levelsHigh-density lipoproteinCross-sectional analysisMetS prevalenceIschemic eventsMetS componentsMetS criteriaWest African populationsMass indexPlasma levelsGhanaian menAntifibrinolytic factors
2015
Treatment with Sildenafil Improves Insulin Sensitivity in Prediabetes: A Randomized, Controlled Trial
Ramirez CE, Nian H, Yu C, Gamboa JL, Luther JM, Brown NJ, Shibao CA. Treatment with Sildenafil Improves Insulin Sensitivity in Prediabetes: A Randomized, Controlled Trial. The Journal Of Clinical Endocrinology & Metabolism 2015, 100: 4533-4540. PMID: 26580240, PMCID: PMC4667163, DOI: 10.1210/jc.2015-3415.Peer-Reviewed Original ResearchMeSH KeywordsAdultAlbuminuriaDouble-Blind MethodEndothelium, VascularFemaleFibrinolysisGlucoseGlucose Clamp TechniqueGlucose Tolerance TestHemodynamicsHumansInsulinInsulin ResistanceMaleMiddle AgedOverweightPhosphodiesterase 5 InhibitorsPlasminogen Activator Inhibitor 1Prediabetic StateSildenafil CitrateConceptsPhosphodiesterase-5 inhibitionGlucose-stimulated insulin secretionInsulin sensitivity indexInsulin sensitivityInsulin secretionBaseline insulin sensitivity indexPlacebo-controlled studyClinical Research CenterBody mass indexEnd of treatmentPlasminogen activator inhibitor-1Tissue plasminogen activatorActivator inhibitor-1Placebo groupUrine albuminSildenafil groupCreatinine ratioEndothelial functionPrimary outcomeMass indexTreatment armsFibrinolytic balanceDisposition indexHyperglycemic clampOverweight individualsGenetics of Plasminogen Activator Inhibitor-1 (PAI-1) in a Ghanaian Population
White MJ, Kodaman NM, Harder RH, Asselbergs FW, Vaughan DE, Brown NJ, Moore JH, Williams SM. Genetics of Plasminogen Activator Inhibitor-1 (PAI-1) in a Ghanaian Population. PLOS ONE 2015, 10: e0136379. PMID: 26322636, PMCID: PMC4556460, DOI: 10.1371/journal.pone.0136379.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Genetic variantsCircadian clock genesMost genetic studiesCardiovascular disease susceptibilityImportant genetic variantsActivator inhibitor-1Inhibitor-1Clock genesGenetic studiesGenetic effectsDisease susceptibilityArylsulfatase BMajor modulatorNovel associationsLack of overlapGenesPathway effectsMedian PAI-1European descentVariantsGeneticsPopulationSNPsCaucasian population
2014
Study of Associated Genetic Variants in Indian Subjects Reveals the Basis of Ethnicity Related Differences in Susceptibility to Venous Thromboembolism
Kumari B, Srivastava S, Chatterjee T, Vardhan R, Tyagi T, Gupta N, Sahu A, Chandra K, Ashraf M. Study of Associated Genetic Variants in Indian Subjects Reveals the Basis of Ethnicity Related Differences in Susceptibility to Venous Thromboembolism. Thrombosis 2014, 2014: 182762. PMID: 25349733, PMCID: PMC4198785, DOI: 10.1155/2014/182762.Peer-Reviewed Original ResearchProthrombin 20210G/AGenetic variantsAssociated genetic variantsTissue factor pathway inhibitorT mutationCandidate genesGenesMutationsPlasminogen activator inhibitor-1Protective variantsPathway inhibitorActivator inhibitor-1Inhibitor-1Susceptibility of individualsPCR-RFLPFactor pathway inhibitorSusceptibility of IndiansVariantsSusceptibilityMTHFR geneInhibitors
2013
Vitronectin Inhibits Efferocytosis through Interactions with Apoptotic Cells as well as with Macrophages
Bae H, Tadie J, Jiang S, Park D, Bell C, Thompson L, Peterson C, Thannickal V, Abraham E, Zmijewski J. Vitronectin Inhibits Efferocytosis through Interactions with Apoptotic Cells as well as with Macrophages. The Journal Of Immunology 2013, 190: 2273-2281. PMID: 23345331, PMCID: PMC3577940, DOI: 10.4049/jimmunol.1200625.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAnimalsAntibodiesApoptosisBronchoalveolar Lavage FluidCell CountCoculture TechniquesFemaleLipopolysaccharidesMacrophages, PeritonealMaleMiceMice, Inbred C57BLMice, KnockoutNeutrophilsPhagocytosisPlasminogen Activator Inhibitor 1Receptors, Urokinase Plasminogen ActivatorThymocytesVitronectinConceptsUrokinase-type plasminogen activator receptorApoptotic cellsEffective removal of apoptotic cellsIncubation of apoptotic cellsRemoval of apoptotic cellsPhagocytosis of apoptotic cellsSurface of apoptotic cellsIngest apoptotic cellsApoptotic target cellsPurified vitronectinSoluble urokinase-type plasminogen activator receptorEffects of vitronectinEngulfing phagocytesWild typePlasminogen activator inhibitor-1Plasminogen activator receptorVitronectinInhibit phagocytosisApoptotic neutrophilsActivator inhibitor-1Acute inflammatory conditionsInhibitory effectLPS-induced ALIVitronectin-deficientBronchoalveolar lavage
2012
Pathogenetic and predictive value of biomarkers in patients with ALI and lower severity of illness: results from two clinical trials
Agrawal A, Zhuo H, Brady S, Levitt J, Steingrub J, Siegel MD, Soto G, Peterson MW, Chesnutt MS, Matthay MA, Liu KD. Pathogenetic and predictive value of biomarkers in patients with ALI and lower severity of illness: results from two clinical trials. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2012, 303: l634-l639. PMID: 22865551, PMCID: PMC3469636, DOI: 10.1152/ajplung.00195.2012.Peer-Reviewed Original ResearchMeSH KeywordsAcute Lung InjuryAdultAgedAPACHEBiomarkersBronchoalveolar Lavage FluidCohort StudiesFemaleHumansInterleukin-6Interleukin-8MaleMiddle AgedPlasminogen Activator Inhibitor 1PneumoniaPredictive Value of TestsProtein CPulmonary EdemaRespiratory Distress SyndromeRespiratory InsufficiencyRisk FactorsSeverity of Illness IndexThrombomodulinConceptsAcute lung injuryVentilator-free daysPlasma plasminogen activator inhibitor-1IL-6Oxygenation indexClinical trialsPredictive valueClinical outcomesIL-8Treatment of ALIHigher APACHE II scoreHigher plasma IL-6Severe acute lung injuryRelevant outcomesBronchoalveolar lavage (BAL) biomarkersAPACHE II scorePlasma IL-6Cohort of patientsMarker of severitySimilar baseline characteristicsPoor clinical outcomePlasminogen activator inhibitor-1Future clinical trialsAssociation of plasmaActivator inhibitor-1Comparative Effects of Angiotensin Receptor Blockade and ACE Inhibition on the Fibrinolytic and Inflammatory Responses to Cardiopulmonary Bypass
Billings F, Balaguer J, Yu C, Wright P, Petracek M, Byrne J, Brown N, Pretorius M. Comparative Effects of Angiotensin Receptor Blockade and ACE Inhibition on the Fibrinolytic and Inflammatory Responses to Cardiopulmonary Bypass. Clinical Pharmacology & Therapeutics 2012, 91: 1065-1073. PMID: 22549281, PMCID: PMC3822756, DOI: 10.1038/clpt.2011.356.Peer-Reviewed Original ResearchMeSH KeywordsAgedAngiotensin II Type 1 Receptor BlockersAngiotensin-Converting Enzyme InhibitorsBenzimidazolesBiphenyl CompoundsBlood TransfusionBradykininCardiopulmonary BypassEndpoint DeterminationFemaleFibrinolysisHematocritHospital MortalityHumansInflammationInterleukinsLength of StayMaleMiddle AgedMonitoring, IntraoperativePerioperative CarePostoperative ComplicationsRamiprilTetrazolesTreatment OutcomeConceptsAngiotensin II type 1 receptor blockadeACE inhibitionCardiopulmonary bypassReceptor blockadeInflammatory responseType 1 receptor blockadeTissue-type plasminogen activator concentrationAngiotensin receptor blockadeEffect of angiotensinRed cell transfusionDay of surgeryPlasminogen activator inhibitor-1Activator inhibitor-1Plasminogen activator concentrationsHospital stayPlasma transfusionIL-10ACE inhibitorsIL-8Intraoperative fibrinolysisFibrinolysisInhibitor-1Comparative effectsPlaceboTransfusionDifferential Effects of Nebivolol and Metoprolol on Insulin Sensitivity and Plasminogen Activator Inhibitor in the Metabolic Syndrome
Ayers K, Byrne LM, DeMatteo A, Brown NJ. Differential Effects of Nebivolol and Metoprolol on Insulin Sensitivity and Plasminogen Activator Inhibitor in the Metabolic Syndrome. Hypertension 2012, 59: 893-898. PMID: 22353614, PMCID: PMC3402551, DOI: 10.1161/hypertensionaha.111.189589.Peer-Reviewed Original ResearchConceptsEffects of nebivololMetabolic syndromeBlood pressureInsulin sensitivityPlasminogen activator inhibitorAntagonist metoprololGlucose homeostasisThird-generation β-blockerActivator inhibitorMarkers of fibrinolysisCongestive heart failureDiastolic blood pressureLower blood pressureSystolic blood pressureCoronary artery diseaseGlucose tolerance testLarge clinical trialsDetrimental metabolic effectsPlasminogen activator inhibitor-1Insulin sensitivity indexAcute insulin responseΒ-cell functionActivator inhibitor-1Study drugArtery disease
2011
Prospective study of the incidence and predictors of thrombus in children undergoing palliative surgery for single ventricle physiology
Todd Tzanetos DR, Yu C, Hernanz-Schulman M, Barr FE, Brown NJ. Prospective study of the incidence and predictors of thrombus in children undergoing palliative surgery for single ventricle physiology. Intensive Care Medicine 2011, 38: 105-112. PMID: 21979273, PMCID: PMC4747610, DOI: 10.1007/s00134-011-2378-y.Peer-Reviewed Original ResearchMeSH KeywordsBiomarkersCentral Nervous SystemChild, PreschoolFemaleHeart Defects, CongenitalHeart VentriclesHospitals, PediatricHumansInfantInfant, NewbornMaleMedical AuditPalliative CarePerioperative CarePostoperative ComplicationsPredictive Value of TestsProspective StudiesTennesseeThrombosisUltrasonographyConceptsSingle ventricle physiologyTissue plasminogen activator antigenCardiopulmonary bypass timePlasminogen activator antigenPlasma antithrombin IIIVentricle physiologyAntithrombin IIIBypass timePalliative surgeryVentricular functionTissue plasminogen activator antigen concentrationAortic cross-clamp timeCentral venous catheter daysLonger cardiopulmonary bypass timePoor preoperative ventricular functionPredictors of thrombusPreoperative ventricular functionChest tube outputCross-clamp timeBiomarkers of coagulationBlood product administrationLow antithrombin IIICentral venous systemIntensive care unitPlasminogen activator inhibitor-1Epistatic Interactions in Genetic Regulation of t-PA and PAI-1 Levels in a Ghanaian Population
Penrod NM, Poku KA, Vaughn D, Asselbergs FW, Brown NJ, Moore JH, Williams SM. Epistatic Interactions in Genetic Regulation of t-PA and PAI-1 Levels in a Ghanaian Population. PLOS ONE 2011, 6: e16639. PMID: 21304999, PMCID: PMC3031598, DOI: 10.1371/journal.pone.0016639.Peer-Reviewed Original ResearchConceptsEpistatic interactionsPAI-1 levelsRenin-angiotensin systemMultiple genetic effectsPathway-specific genesD polymorphismPAI-1Genetic architectureT-PASingle SNP analysisGenetic regulationCentral genesSpecific genesCardiovascular diseaseFibrinolytic systemSNP analysisGenetic effectsGenesCleavage of angiotensinogenPlasminogen activator inhibitor-1Plasma t-PAT-PA levelsTissue plasminogen activatorActivator inhibitor-1Enzyme cleavage
2010
Leiomyoma Simultaneously Impair Endometrial BMP-2-Mediated Decidualization and Anticoagulant Expression through Secretion of TGF-β3
Sinclair DC, Mastroyannis A, Taylor HS. Leiomyoma Simultaneously Impair Endometrial BMP-2-Mediated Decidualization and Anticoagulant Expression through Secretion of TGF-β3. The Journal Of Clinical Endocrinology & Metabolism 2010, 96: 412-421. PMID: 21084396, PMCID: PMC3048319, DOI: 10.1210/jc.2010-1450.Peer-Reviewed Original ResearchMeSH KeywordsAdultAntithrombin IIIBlood CoagulationBone Morphogenetic Protein 2Cells, CulturedDeciduaDNA, ComplementaryEnzyme-Linked Immunosorbent AssayFemaleHumansImmunohistochemistryInfertility, FemaleLeiomyomaMenorrhagiaMiddle AgedPlasminogen Activator Inhibitor 1Reverse Transcriptase Polymerase Chain ReactionRNAStromal CellsThrombomodulinTransforming Growth Factor beta3Uterine NeoplasmsConceptsEndometrial stromal cellsAntithrombin IIIPAI-1Bone morphogenetic protein receptorTGF-β3Primary endometrial stromal cellsEffects of leiomyomaReproductive-age womenPlasminogen activator inhibitor-1Expression of HOXA10TGF-β3 treatmentEndometrial gene expressionUniversity Medical CenterLess PAI-1Activator inhibitor-1Endometrial defectQuantitative RT-PCREndometrial decidualizationMenstrual bleedingLIF expressionMiscarriage riskUterine leiomyomaMedical CenterReproductive dysfunctionCase controlReview: Therapeutic potential of plasminogen activator inhibitor-1 inhibitors
Brown NJ. Review: Therapeutic potential of plasminogen activator inhibitor-1 inhibitors. Therapeutic Advances In Cardiovascular Disease 2010, 4: 315-324. PMID: 20660535, DOI: 10.1177/1753944710379126.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Plasminogen Activator Inhibitor-1 InhibitorsInitiation of diabetesPathogenesis of thrombosisPotential therapeutic strategyActivator inhibitor-1Major physiological inhibitorRenal injuryVascular remodelingPreclinical studiesTherapeutic strategiesSmall molecule inhibitorsTherapeutic potentialInhibitor-1Physiological inhibitorMolecule inhibitorsCell migrationInhibitorsThrombosisDiabetesFibrosisPathogenesisFibrinolysisInjuryDisease
2009
Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction
Ma H, Saenko M, Opuko A, Togawa A, Soda K, Marlier A, Moeckel GW, Cantley LG, Ishibe S. Deletion of the Met receptor in the collecting duct decreases renal repair following ureteral obstruction. Kidney International 2009, 76: 868-876. PMID: 19675527, DOI: 10.1038/ki.2009.304.Peer-Reviewed Original ResearchConceptsUreteral obstructionFibrotic responseKnockout miceMet receptorAcute tubular necrosisPlasminogen activator inhibitor-1Unilateral ureteral obstructionTubular cell proliferationActivator inhibitor-1Conditional knockout miceHepatocyte growth factorKidney injuryRenal injuryTubular necrosisFunctional recoveryInterstitial fibrosisCre miceRenal repairNephron injuryControl littermatesObstructionGrowth factorMiceInhibitor-1InjuryRole of the syncytium in placenta-mediated complications of preeclampsia
Guller S. Role of the syncytium in placenta-mediated complications of preeclampsia. Thrombosis Research 2009, 124: 389-392. PMID: 19535132, PMCID: PMC2764997, DOI: 10.1016/j.thromres.2009.05.016.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Fms-like tyrosine kinase-1Complications of preeclampsiaIntrauterine growth restrictionPathophysiology of preeclampsiaTyrosine kinase-1Immune cell functionAnti-angiogenic factorsActivator inhibitor-1Potential protective actionMaternal hemostasisSoluble endoglinEndothelial functionReperfusion injuryMaternal endotheliumMaternal mortalityRelease of microparticlesGrowth restrictionMaternal bloodPreeclampsiaSensitive markerMajor causeInhibitor-1Protective actionReactive oxygen speciesAldosterone antagonism or synthase inhibition reduces end-organ damage induced by treatment with angiotensin and high salt
Lea WB, Kwak ES, Luther JM, Fowler SM, Wang Z, Ma J, Fogo AB, Brown NJ. Aldosterone antagonism or synthase inhibition reduces end-organ damage induced by treatment with angiotensin and high salt. Kidney International 2009, 75: 936-944. PMID: 19225557, PMCID: PMC2770712, DOI: 10.1038/ki.2009.9.Peer-Reviewed Original ResearchConceptsAldosterone synthase inhibitionEnd-organ damageHigh salt intakeWeeks of treatmentPlasminogen activator inhibitor-1Angiotensin IISynthase inhibitionMRNA expressionSalt intakeInterstitial fibrosisGrowth factor-beta mRNA expressionAortic medial hypertrophyMineralocorticoid receptor blockadeMineralocorticoid receptor antagonismHigh-salt dietCardiac interstitial fibrosisKidneys of ratsPAI-1 mRNA expressionActivator inhibitor-1MRNA protein expressionAldosterone antagonismHypertensive responseRenal effectsUninephrectomized ratsMedial hypertrophy
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