Featured Publications
Smooth Muscle Mineralocorticoid Receptor Promotes Hypertension After Preeclampsia
Biwer L, Lu Q, Ibarrola J, Stepanian A, Man J, Carvajal B, Camarda N, Zsengeller Z, Skurnik G, Seely E, Karumanchi S, Jaffe I. Smooth Muscle Mineralocorticoid Receptor Promotes Hypertension After Preeclampsia. Circulation Research 2023, 132: 674-689. PMID: 36815487, PMCID: PMC10119809, DOI: 10.1161/circresaha.122.321228.Peer-Reviewed Original ResearchConceptsBlood pressureSMC-MRHypertensive stimuliBP responseSmooth Muscle Cell Mineralocorticoid ReceptorsAngII type 1 receptorType 1 receptor expressionMR transcriptional activityIncreased cardiovascular riskElevated blood pressureEnd-organ damageHigh salt intakeHigh blood pressureRisk of hypertensionType 1 receptorSoluble VEGF receptorAngII infusionPrior preeclampsiaMR antagonismCardiovascular riskNormotensive pregnanciesSalt dietAortic stiffnessSalt intakeOrgan damage
2019
Gradual hypertension induction in middle‐aged Cyp1a1‐Ren2 transgenic rats produces significant impairments in spatial learning
Willeman M, Chawla M, Zempare M, Biwer L, Hoang L, Uprety A, Fitzhugh M, De Both M, Coleman P, Trouard T, Alexander G, Mitchell K, Barnes C, Hale T, Huentelman M. Gradual hypertension induction in middle‐aged Cyp1a1‐Ren2 transgenic rats produces significant impairments in spatial learning. Physiological Reports 2019, 7: e14010. PMID: 30916484, PMCID: PMC6436186, DOI: 10.14814/phy2.14010.Peer-Reviewed Original ResearchConceptsTransgenic ratsBlood pressureCyp1a1-Ren2 transgenic ratsRenin-dependent hypertensionImpact of hypertensionInduction of hypertensionSystolic blood pressureTransgenic rat modelMajor health concernAge of onsetRenal hypertrophyPrevalence increasesHypertension inductionRat modelHypertensionNeurological healthCollagen depositionLeft ventricleSensory functionBrain regionsCardiovascular systemSignificant impairmentRate of inductionMorris swim taskRats
2015
Persistent change in cardiac fibroblast physiology after transient ACE inhibition
D'Souza K, Biwer L, Madhavpeddi L, Ramaiah P, Shahid W, Hale T. Persistent change in cardiac fibroblast physiology after transient ACE inhibition. AJP Heart And Circulatory Physiology 2015, 309: h1346-h1353. PMID: 26371174, DOI: 10.1152/ajpheart.00615.2015.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme InhibitorsAnimalsCardiomyopathiesCell ProliferationCells, CulturedChemokine CCL2Collagen Type IDisease Models, AnimalEnalaprilFibroblastsFibrosisGranulocyte-Macrophage Colony-Stimulating FactorHeart VentriclesHypertensionInflammation MediatorsMaleNG-Nitroarginine Methyl EsterNitric Oxide SynthasePhenotypeRats, Inbred SHRTime FactorsConceptsTransient ACE inhibitionACE inhibitionFibroblast physiologyArginine methyl ester treatmentCardiac fibroblastsAngiotensin-converting enzyme inhibitionPersistent changesMethyl ester treatmentChemoattractant protein-1Granulocyte macrophage-colony stimulating factorArginine methyl esterMacrophage-colony stimulating factorMacrophage-recruiting chemokinesCardiac fibroblast phenotypeRole of fibroblastsUntreated SHRHypertensive ratsNOS inhibitionWashout periodACE inhibitorsCardioprotective effectsChemokine releaseMyocardial injuryCardiac fibrosisNOS inhibitor
2012
Protection against L‐NAME‐induced reduction in cardiac output persists even after cessation of angiotensin‐converting enzyme inhibitor treatment
Biwer L, Broderick T, Xu H, Carroll C, Hale T. Protection against L‐NAME‐induced reduction in cardiac output persists even after cessation of angiotensin‐converting enzyme inhibitor treatment. Acta Physiologica 2012, 207: 156-165. PMID: 22834875, DOI: 10.1111/j.1748-1716.2012.02474.x.Peer-Reviewed Original ResearchConceptsL-NAMEMyocardial injuryCardiac functionEnalapril treatmentACE inhibitionCardiac outputL ratsL-NAME-induced reductionNitric oxide synthase inhibitorShort-term angiotensinTransient ACE inhibitionEnzyme inhibitor treatmentHeart failure treatmentCessation of treatmentOxide synthase inhibitorArginine methyl esterEosin-stained sectionsArterial pressureHypertensive ratsCardiac changesCardiac dysfunctionWashout periodCoronary flowMyocardial infarctionFailure treatment