2021
Mineralocorticoid Receptor in Smooth Muscle Contributes to Pressure Overload–Induced Heart Failure
Kim S, Biwer L, Moss M, Man J, Aronovitz M, Martin G, Carrillo-Salinas F, Salvador A, Alcaide P, Jaffe I. Mineralocorticoid Receptor in Smooth Muscle Contributes to Pressure Overload–Induced Heart Failure. Circulation Heart Failure 2021, 14: e007279. PMID: 33517669, PMCID: PMC7887087, DOI: 10.1161/circheartfailure.120.007279.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsMR-intact littermatesAdverse cardiac remodelingMineralocorticoid receptorCardiac remodelingSMC-MRAortic constrictionPressure Overload-Induced Heart FailureInhibition of MRRole of MRPressure overload-induced hypertrophyCardiac blood supplyHeart failure hospitalizationCardiac capillary densityCoronary flow reserveTransverse aortic constrictionIntracardiac pressure measurementsOverload-induced hypertrophyFibrotic gene expressionFetal gene expressionFailure hospitalizationExercise capacityExercise testingEjection fractionHeart failure
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