2013
Centrally administered angiotensin‐(1–7) increases the survival of stroke‐prone spontaneously hypertensive rats
Regenhardt RW, Mecca AP, Desland F, Ritucci‐Chinni P, Ludin JA, Greenstein D, Banuelos C, Bizon JL, Reinhard MK, Sumners C. Centrally administered angiotensin‐(1–7) increases the survival of stroke‐prone spontaneously hypertensive rats. Quarterly Journal Of Experimental Physiology And Cognate Medical Sciences 2013, 99: 442-453. PMID: 24142453, PMCID: PMC7416533, DOI: 10.1113/expphysiol.2013.075242.Peer-Reviewed Original ResearchConceptsHaemorrhagic strokeHypertensive ratsMicroglial activationIschemic strokeNeurological statusTherapeutic targetBeneficial actionsInfusion of AngMas receptor blockerHigh sodium dietPotential new therapeutic targetAction of angiotensinNumber of microgliaMechanism of injuryNumber of hemorrhagesSerum corticosterone levelsActivation of angiotensinPotential therapeutic targetNew therapeutic targetsPotential beneficial actionsPotential beneficial roleDays of ageAng-(1-7) treatmentIntracerebral inflammationMicroglial numbers
2006
Prevention of angiotensin II-induced cardiac remodeling by angiotensin-(1–7)
Grobe JL, Mecca AP, Lingis M, Shenoy V, Bolton TA, Machado JM, Speth RC, Raizada MK, Katovich MJ. Prevention of angiotensin II-induced cardiac remodeling by angiotensin-(1–7). AJP Heart And Circulatory Physiology 2006, 292: h736-h742. PMID: 17098828, DOI: 10.1152/ajpheart.00937.2006.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAngiotensin IAngiotensin IIAnimalsBlood PressureCardiomegalyDisease Models, AnimalFibrosisHeartHypertensionMaleMyocardiumPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsRatsRats, Sprague-DawleyReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptors, G-Protein-CoupledTime FactorsTransforming Growth Factor betaVentricular RemodelingConceptsRenin-angiotensin systemCardiac remodelingChronic infusionBlood pressureAng IIHeart failureInterstitial fibrosisAngiotensin IIMyocyte hypertrophyHyperactive renin-angiotensin systemAng II type 1Adult Sprague-Dawley ratsEffects of AngSubsequent heart failureOverexpression of angiotensinAcute myocardial infarctionMajor risk factorFormation of AngSprague-Dawley ratsCardiac tissueSubgroup of animalsChronic hypertensionAng receptorsMyocardial infarctionRisk factors
2005
Protection from angiotensin II‐induced cardiac hypertrophy and fibrosis by systemic lentiviral delivery of ACE2 in rats
Huentelman MJ, Grobe JL, Vazquez J, Stewart JM, Mecca AP, Katovich MJ, Ferrario CM, Raizada MK. Protection from angiotensin II‐induced cardiac hypertrophy and fibrosis by systemic lentiviral delivery of ACE2 in rats. Quarterly Journal Of Experimental Physiology And Cognate Medical Sciences 2005, 90: 783-790. PMID: 16049057, DOI: 10.1113/expphysiol.2005.031096.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IIAngiotensin-Converting Enzyme 2AnimalsAnimals, NewbornBlood PressureBody WeightCarboxypeptidasesCardiomyopathy, HypertrophicEndomyocardial FibrosisGene ExpressionGenetic VectorsHeartLentivirusMiceMyocardiumOrgan SizePeptidyl-Dipeptidase ARatsRats, Sprague-DawleyTransduction, GeneticConceptsRenin-angiotensin systemAngiotensin IIMyocardial fibrosisCardiac hypertrophyAngiotensin II infusionSystolic blood pressureBody weight ratioOverexpression of ACE2Potential therapeutic targetII infusionMmHg increaseBlood pressureHeart weightControl ratsDawley ratsCardiovascular diseaseEnzyme 2Protective effectTherapeutic targetMouse ACE2FibrosisHypertrophyRatsACE2Significant attenuation