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 numbersAnti-inflammatory effects of angiotensin-(1-7) in ischemic stroke
Regenhardt RW, Desland F, Mecca AP, Pioquinto DJ, Afzal A, Mocco J, Sumners C. Anti-inflammatory effects of angiotensin-(1-7) in ischemic stroke. Neuropharmacology 2013, 71: 154-163. PMID: 23583926, PMCID: PMC3664115, DOI: 10.1016/j.neuropharm.2013.03.025.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IAnimalsAnti-Inflammatory Agents, Non-SteroidalBrain IschemiaCells, CulturedCerebral CortexDisease Models, AnimalGene Expression RegulationMaleMiceMice, Inbred StrainsMice, KnockoutMicrogliaNerve Tissue ProteinsNeuroprotective AgentsNitric OxideNitric Oxide Synthase Type IIPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledSpecific Pathogen-Free OrganismsStrokeConceptsInducible nitric oxide synthaseAnti-inflammatory effectsIschemic strokeEndothelin-1Cerebral cortexMiddle cerebral artery occlusionCerebral infarct sizeDifferentiation molecule 11bIntracerebral inflammatory responseCerebral artery occlusionAnti-inflammatory actionLipopolysaccharide-induced increasePro-inflammatory cytokinesCerebral blood flowINOS protein expressionNitric oxide synthaseNitric oxide productionNitric oxide generationExpression of mRNAAng-(1-7) treatmentSignificant cerebroprotectionCerebral vasoconstrictionArtery occlusionCerebroprotective actionReceptor Mas
2011
Cerebroprotection by angiotensin‐(1–7) in endothelin‐1‐induced ischaemic stroke
Mecca AP, Regenhardt RW, O’Connor T, Joseph JP, Raizada MK, Katovich MJ, Sumners C. Cerebroprotection by angiotensin‐(1–7) in endothelin‐1‐induced ischaemic stroke. Quarterly Journal Of Experimental Physiology And Cognate Medical Sciences 2011, 96: 1084-1096. PMID: 21685445, PMCID: PMC3210510, DOI: 10.1113/expphysiol.2011.058578.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin IAngiotensin IIAngiotensin-Converting Enzyme 2AnimalsDiminazeneEndothelin-1Enzyme ActivationInfarction, Middle Cerebral ArteryMaleNitric Oxide Synthase Type IIPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledStrokeConceptsMiddle cerebral artery occlusionIschemic strokeDiminazine aceturateNeurological deficitsBeneficial actionsInducible nitric oxide synthase (iNOS) expressionInducible nitric oxide synthase (iNOS) mRNA expressionNitric oxide synthase mRNA expressionNitric oxide synthase expressionCerebral infarct sizeCerebral artery occlusionCerebral ischemic strokeOxide synthase expressionCerebral blood flowExert beneficial actionsType 1 receptorActivation of angiotensinSynthase mRNA expressionACE2 activatorACE2-AngCerebroprotective propertiesDIZE treatmentCerebral infarctsProduction of angiotensinArtery occlusion
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 factorsChronic angiotensin-(1–7) prevents cardiac fibrosis in DOCA-salt model of hypertension
Grobe JL, Mecca AP, Mao H, Katovich MJ. Chronic angiotensin-(1–7) prevents cardiac fibrosis in DOCA-salt model of hypertension. AJP Heart And Circulatory Physiology 2006, 290: h2417-h2423. PMID: 16415071, DOI: 10.1152/ajpheart.01170.2005.Peer-Reviewed Original ResearchConceptsDOCA-salt modelBlood pressureCardiac hypertrophyCardiac fibrosisCardiac remodelingDeoxycorticosterone acetate pelletsDOCA-salt animalsBlood pressure responseCarotid artery cannulationDOCA-salt treatmentTail-cuff methodWk of treatmentPerivascular collagen depositionSprague-Dawley ratsNormal drinking waterAngiotensin fragmentsChronic angiotensinDOCA animalsAngiotensin infusionArtery cannulationPerivascular fibrosisSham surgeryAngiotensin IIOsmotic minipumpsMyocyte diameter