简介：AbstractIntroduction:Tripterygium glycosides (TGs) have been widely used in China to treat diabetic nephropathy (DN); however, proof of their use is scarce. The present study aimed to evaluate the effectiveness and safety of adding TGs to angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).Methods:By searching Embase, MEDLINE, Cochrane Library, SINOMED, China National Knowledge Infrastructure, VIP Information/Chinese Scientific Journals, and WANFANG databases, we identified previous studies that met the specific selection criteria and included them in the meta-analysis. Analyses were performed using Review Manager (version 5.3).Results:Nine randomized controlled trials were included in the final meta-analysis. Patients were compared before and after treatment with ACE inhibitors or ARBs plus TGs, or ACE inhibitors or ARBs alone. The results revealed that treatment with ACE inhibitors or ARBs plus TGs resulted in significantly greater reductions in 24-h urinary total protein (UTP) levels (trial duration <2 months, mean difference [MD]: -0.25; 95% confidence interval [CI]: -0.32, -0.18; trial duration between 2 and 6 months, MD: -0.39; 95% CI: -0.44, -0.33; trial duration >6 months, MD: -2.09; 95% CI: -2.89, -1.29) compared with treatment using ACE inhibitors or ARBs alone. Additionally, ACE inhibitors or ARBs plus TGs showed better results after longterm administration. Treatment with ACE inhibitors or ARBs plus TGs resulted in significantly greater reductions in serum creatinine (SCr) compared with ACE inhibitors or ARBs alone (MD: -9.87; 95% CI: -13.76, -5.97).Conclusion:In patients with DN, adding TGs to ACE inhibitors or ARBs significantly lowered both the 24-h UTP and SCr levels. Therefore, ACE inhibitors or ARBs plus TGs might improve the treatment of DN in patients.

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简介：ObjectiveThestudywillexploreeffectsoftheautoantibodiesagainstAT1receptorandangiotensinⅡontherefractoryhypertension.MethodsSeventy-sevenpatients(46menand31women)withessentialhypertensionweredividedintogroupsofrefractoryhypertension(RH)andhypertension(HT)accordingtothe1999WHO-ISHGuidelinesfortheManagementofHypertension.Fortynormotensives(22men)wererecruitedascontrols.Themeanagewas54.3±13yearsoldinRHgroup,53.5±9yearsoldinHTgroupand51.2±11.9yearsoldinnormotensives(NT)group.Themeanbloodpressurewas154.2±9.4/98.4±8.2mmHginRHgroupand130.1±7.6/80.5±6.7mmHginHTgroupaftercombinationdrugtherapyofhypertensionfor4weeks.BloodpressureinNTgroupwas120.8±11.7/76.4±7.2mmHg.Theepitopeofthe2ndextracellularloopsofAT1receptorwassynthesizedandusedasantigenstoscreentheautoantibodiesbyELISA.Plasmaangiotensin(Ang)IIwereexaminedbyaradioimmunoassay.ResultsT

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简介：ObjectivesTostudythechangesofnitricoxide,angiotensinⅡandsuperoxideanioninrenalarteryhypertensionpathogenesis.MethodsMaleWistarratsweighing256-285gweredividedinto5groupsrandomly,10ratsofeachgroup.Controlgroup:falseoperationwasmadeandroutinedietwasgiven;Ligaturegroup:leftrenalarterywasligatureduncompletelyandroutinedietwasgiven;Ligature+Losartangroup:leftrenalarterywasligatureduncompletelyandLosartan20mg·kg^-1·d^-1wasaddedinthedrinkingwater;Ligature+L-Arggroup:leftrenalarterywasligatureduncompletelyandL-Arg2g·kg^-1·d^-1wasaddedinthedrinkingwater;Ligature+L-Arg+Losartangroup:leftrenalarterywasligatureduncompletelyandL-Arg2g·kg^-1·d^-1andLosartan20mg·kg^-1·d^-1wasaddedinthedrinkingwater.Bloodpressureandheartrateweremeasuredbeforeandattheendoftheexperiment.Oneweekafterligature,bloodwasdrawntodetermineangiotensinⅡ,cGMP,nitricoxide,nitricoxidesynthase(NOS),O2^-,superoxidedismutase(SOD).ResultsSystolicbloodpressurewashigherinligaturegroupthanthatincontrolgroup(p<0.05),systolicbloodpressurewasmuchlowerinligature+Losartangroupthanthatinligaturegroup.Heartratedidnotchangesignificantlyafterexperiment(p>0.05).AngⅡwashigherinligaturegroupthanthatincontrolgroup,evenmuchhigherinligature+Losartangroup(p<0.01).TherewasnodifferenceofcGMPineachgroup(p>0.05).TheconcentrationofNOwaslowerinligaturegroup(p<0.05),NOwashigherinligature+L-Arg+Losartangroupthanthatinligaturegroup(p<0.05).O2^-washigherinligaturegroupandligature+L-Arggroupthanthatincontrolgroup(p<0.05),O2^-waslowerinligature+Losartangroupthanthatinligaturegroup(p<0.05).ThelevelofSODwaslowerinligaturegroupthanthatincontrolgroup(p<0.05),higherinligature+L-Arggroupandligature+L-Arg+Losartangroupthanthatinligature

简介：backgroundIt'sestablishedthatAngiotensinⅡanditsreceptorsareinvolvedinintimalhyperplasiaafterballooninjuryandstentrestenosis.Recentevidencealsosuggeststhatstatinshavesomeanti-intimalhyperplasiaeffects.Inthisstudy,theeffectofRosuvastatinonexpressionofangiotensinⅡreceptorsinrataorticendotheliumafterballooninjuryisthereforeinvestigated.MethodsAll52WistarKyotoratswereestablishedtoaortainjurymodelsby2Fballooncatheter,thenwererandomlydividedintoshamoperationgroup,aortainjurygroupandRosuvastatin-treatmentgroup.After14days,theaorticspecimensoftheanimalswereharvestedandperformedimmunohistochemistryanddeterminationofmolecularbiology.ResultsTheresultsshowedthat(i)The14days-ballooninjuryinducedobviousintimathickening(P<0.01),however,thephenomenonwasreducedby14days-treatmentwithRosuvastatin(P<0.01).(ii)TheexpressionsofangiotentionⅡtypeⅠ(AT1)andtypeⅡ(AT2)receptormRNAandproteinweremarkedlyup-regulatedbytheballooninjury(P<0.01),after14days-treatmentwithRosuvastatin,theexpressionofAT1receptormRNAanditsproteinwasdecreased(P<0.01),buttheexpressionofAT2receptormRNAanditsproteinwasfurtherincreased(P<0.05).ConclusionInthisstudy,weobservedthattheballooninjuryinduced-intimathickeningwasreducedbyRosuvastatininrats,whichmightbelinkedwiththeregulationofexpressionofangiotensinⅡreceptors.

简介：Inspiteofrecentadvancesintreatmentandcontrol,theprevalenceofCVDandpulmonaryhypertension(PH)aroundtheworldhasincreasedsignificantly.Webelievethataconceptualbreakthroughisneededandnoveldrugtargetsmustbediscoveredinanattempttocontrolandtreatthem.ACE2,thenewestmemberoftherenin-angiotensinsystem(RAS),appearstoholdthispotential.Ourstudieshaveestablishedanovelconcept:abalancebetweenthevasodeleteriousaxis(ACE/AngⅡ/ATlR)andthevasoprotectiveaxis(ACE2/Ang-1-7/Mas)oftheRASiscriticalinmaintainingnormalCVfunctionsandanyimbalanceinitiatesvasculardysfunctionsleadingtocardiopulmonarydiseases.ThuswehypothesizethatACE2,whichisakeyenzymeindecreasingAngⅡandincreasingAng-1-7,wouldbeanidealforconsiderationasatherapeutictarget.Theobjectiveofmypresentationwillbetopresentevidenceinsupportofthisconcept.ThedatapresentedwilldemonstratethatoverexpressionofACE2bygeneticmeansoritsactivationbenovelACE2activatorsproteststheheartfromhypertension-andMi-inducedcardiacdamage.Also,thisstrategyisextremelyeffectiveinpreventionandreversalofPHandpulmonaryfibrosis.Astructure-baseddrugdiscoveryapproachwillbepresentedtoidentifysmallmoleculeACE2acti-vatorsandtheirpotentialinproducingbeneficialoutcomesonCVDandpulmonaryhypertensionwillbediscussed.

简介：Theangiotensin-convertingenzymegeneisacandidategeneofstroke.Thepresentstudyinvolved62healthyvolunteersand148patientswithmiddlecerebralarterystenosisasconfirmedbybraincolorultrasoundfromaHanpopulationinNorthChina,anddeterminedtheperipheralbloodangiotensin-convertingenzymegenotypeusingPCR-restrictionfragmentlengthpolymorphismanalysis.TheresultsshowedthatthefrequenciesoftheDDgenotypeandDallelewereincreasedinpatientswithmiddlecerebralarterystenosis,butthedifferencewasnotstatisticallysignificantcomparedwithhealthycontrols.ThefindingsofthisstudyontherelationshipbetweenstrokegenesandmiddlecerebralarterystenosisindicatenosignificantcorrelationbetweenthefrequenciesoftheDDgenotypeandDalleleofangiotensin-convertingenzymeandmiddlecerebralarterystenosisinthisHanpopulationfromNorthChina.Inthefuture,studieswillbecarriedouttoinvestigatecorrelationsbetweenmultiplestrokecandidategenesynergyandmiddlecerebralarterystenosistoprovideafoundationforthedevelopmentofgenetherapy.

简介：Objective:Toobservethetherapeuticeffectofelectroacupuncture(EA)onplasmaangiotensin(Ang*.Ⅱ),aldosterone(ALD)andatrialnatriureticpolypeptide(ANP)contentsinexperimentalcerebralinfarctionrabbitsforanalyzingtheunderlyingmechanismofacupunctureinamelioratingbloodsupplyofthebraintissue.Methods:Atotalof80rabbitswererandomizedintocontrol(n=8),pseudo-operation(n=24),model(n=24)andEA(n=24)groups.Cerebralinfarctionmodelwasestablishedbyinfusionofself-thrombusintothecarotidartery.EA(1mA,2Hz)wasappliedto'Baihui'(百会GV20)and'Shuigou'(水沟GV26)for30min,onceevery12hours.PlasmaAng-II,ALDandANPcontentsweredetectedwithradioimmunoassaymethod.Inthelater3groups,bloodsamplesweretakenat6h,24hand48haftercerebralischemia.Results:Comparedwithcontrolandpseudo-operationgroups,Ang-IIandALDcontentsofmodelgroupat6h,24hand48haftercerebralischemiaincreasedsignificantlywhileplasmaANPofthe3time-coursesofmodelgroupdecreasedconsiderably(P<0.01).Incomparisonwithmodelgroup,resultsshowedthatAng-IIandALDcontentsofEAgroupdecreasedsignificantlywhereasANPlevelofEAgroupincreasedstrikingly(P<0.01).Conclusion:ElectroacupuncturehastheeffectsofraisingplasmaANPlevelandloweringplasmaAng-IIandALDincerebralinfarctionrabbits.

简介：ObjectivesInvestigatedtheeardioproteetiveandmechanismsoflosartanonwholeisolatedisehemiereperfusedratheart.MethodsLangendorffperfusedsystemswasusedtoinvestigatelosartaneffectonwholeisolatedratheartsinCPK,LDH,MDA,SOD,angⅡandarrhythmia.ResuitsLosartandecreasedincidenceofarrhythmia,improvedatrialventrieularblockrecoveryinreperfusionperiod,duringisehemieperiod,CPKandLDHinI/Rgroupincreasedsignificantlycomparedwithcontrolgroup,51.33±27.02vs22.42±13.33,31.80±4.56vs22.28±15.96,respectively,butgreatlydecreasedinlosartangroupcomparedwithI/Rgroup,23.90±21.74vs51.33±27.02and11.50±13.20vs31.80±4.56,respectively.DuringreperfusionperiodCPK,LDHincreasedsignificantlyinI/Rgroupcomparedwithcontrolgroup,49.11±20.63vs12.14±5.92and28.70±4.69vs23.10±21.38,respectively,butdecreasedgreatlyinlosartangroupcomparedwithI/Rgroup,39.40±9.60vs49.11±20.63and14.50±13.75vs28.70±4.69.ThecontentofMDA,angIIinI/Rgroupmyoeytesishigherthancontrolgroup's,26.±9.25vs17.2±3.37and8.43±3.81vs4.80±0.20.HoweverthecontentofSODintwogroupshasnosignificantlychange,148.20±8.72vs145.08±6.82.thecontentofMDAinlosartangroupmyocardialtissueismuchlowerthancontrolgroup,15.92±4.05vs26.80±9.25andthecontentofangⅡinlosartangroupmyocardialtissueismuchhigherthanI/Rgroup,12.44±6.09vs8.43±3.21.ThedepartmentofcardiologyofsecondhospitalofTianjinmedicaluniversityTianjin300211However,SODhasnosignificantchangeintwogroups,143.47±7.91vs145.08±6.82.ConclusionsLosartanagainstisehemie-reperfusioninjuryofwholeisolatedrathearts,thosebeneficialeffectsaremediateprimarilybytheinhibitedofangiotensinⅡbindingwithitsreceptorandinhibitedoxygenfreeradicalscavengingpotential.

简介：AbstractCoronavirus disease 2019 is a major threat to public health globally. Though its pathogenesis has not been fully elucidated, angiotensin-converting enzyme 2 (ACE2) has been recently identified as a receptor for the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into the cell. Here, we aimed to clarify the potential role of ACE2 in SARS-CoV-2-induced acute lung injury and its underlying mechanism. As a receptor for coronavirus, ACE2 mediates the entry of SARS-CoV-2 into cells in a similar way as for severe acute respiratory syndrome coronavirus (SARS-CoV). The high binding affinity of SARS-CoV-2 to ACE2 correlates with its efficient spread among humans. On the other hand, ACE2 negatively regulates the renin-angiotensin-aldosterone system (RAAS) primarily by converting angiotensin II to angiotensin 1-7, which exerts a beneficial effect on coronavirus-induced acute lung injury. Human recombinant ACE2 has been considered as a potential therapy for SARS-CoV-2 by blocking virus entry and redressing the imbalance of RAAS in SARS-CoV-2 infection. The level of ACE2 expression can be upregulated by treatment with an ACE inhibitor (ACEI) or angiotensin II type 1 receptor blocker (ARB). To date, no evidence shows that ACEIs or ARBs increase the susceptibility and mortality of patients infected with SARS-CoV-2, and hence, it is not advisable to discontinue such drugs in patients with cardiovascular disease.

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简介：ObjectivesToexamineinvivointeractionsbetweenangiotensinⅡ(AngⅡ)AT1areceptor(AT1aR),angiotensin-convertingenzymes(ACE)andACE2usingsmallhairpinRNA(shRNA)gene-silencingmethodsinmicebrainstemnucleustractussolitarius(NTS).MethodsC57BLmice(n=8)wereusedasanimalmodel.MethodofmicroinjectioninthenucleusofNTSwasadopted.Aftertendays,micewerekilledandtheirbraintissuewerefixedandsectioned.TheexpressionlevelsofAT1aR,ACEandACE2mRNAatbothsidesofNTSwereexaminedbyinsituhybridization.Basedoncomparedt-test,thechangingformRNAexpressionwasexamined.ResultsAftertheexpressionofAT1aRmRNAwassignificantlyinhibited(61.6%±6.8%)byAT1aR-shRNA,itwasassociatedwithdecreasesinACE2mRNAexpressionfrom(1.05±0.12)μCi/mgto(0.74±0.09)μCi/mg(29.0%±14.5%,P<0.01)onthesamesideofthebrainstem.ACEmRNAexpressionwasconsistentatbothsides(0.50μCi/mg±0.09μCi/mgand0.53μCi/mg±0.08μCi/mg),withinsignificantdifference(P>0.05).ConclusionsThegenesilencingresultshowedthattherewereinteractionsbetweenbrainstemAT1aRandACE2.ACEmRNAexpressionwasnotalteredbyRNAinterferencetreatmentatAT1aR.

简介：Toobtainthemaximumangiotensin-Iconvertingenzyme(ACE)inhibitoryactivity,theproteinhydrolysisconditionsofthejellyfishRhopilemahispidumwereoptimizedusingresponsesurfacemethodology(RSM).TrypsinwasselectedtoproduceR.hispidumproteinhydrolysates(RPH)withACEinhibitoryactivity.TheoptimalparametersforproducingproteinhydrolysateswiththehighestACEinhibitoryactivitywereasfollows:hydrolysistime5h,hydrolysistemperature50℃,andtheenzyme-to-substrateratio6%.Undertheseconditions,theACEinhibitoryrateofRPHcouldreach64.28%±5.72%.Inaddition,RPHcontainedhighlevelsofGly,Glu,Pro,Ala,AspandArg,withamolecularweightdistributionrangeof0.32–6.84kDa.ThefollowingthreenovelACEinhibitorypeptideswereisolatedandidentified:Ile-Gly-Glu-Thr-Gly-Pro,Gly-Ala-Thr-Gly-Pro-Ala-Gly-Tyr-ValandGly-Ala-Phe-Gly-Pro-Gly-Gly-Leu-Val-Gly-Arg-Pro.TheIC50valuesoftheACEinhibitoryactivityofthesethreepurifiedpeptideswere19.07,27.42and31.26μmolL^-1,respectively.TheseresultssuggestedthatproteinsandpeptidesisolatedfromR.hispidumcouldbeutilizedasantihypertensivefunctionalfoodsources.

简介：BackgroundEssentialhypertension(EH)isconsideredtobeoneofthemostimportantriskfactorofischemicstroke.Studiesaboutriskfactorsinthepatientsaremeaningfulinearlyforecastandeffectivepreventionoftheonsetofstroke.Renin-angiotensin-aldosteronesystemplaysanimportantroleintheregulationofbloodpressureandthedevelopmentofstroke,whilerecentstudieshavefoundthattheangiotensin-convertingenzyme2(ACE2)maybeareversalagentforthedevelopmentandprogressionofischemicstroke.MethodsTheACE2genewasmeasuredin139EHpatientswithischemicstrokeusingpolymerasechainreaction(PCR)andrestrictionfragmentlengthpolymorphism(PCR-RFLP)tests.Detailedandcompleteclinicalandbiochemicaldatawerecollected,includingpulsepressure,hsCRP,IMT,HDL-Canduricacidlevels.Studythecorrelationbetweenangiotensin-convertingenzyme2geneandtheriskfactorforonsetofischemicstrokeinEHpatients.ResultsPulsepressure,hsCRP,IMTanduricacidlevelshadapositivecorrelationwithon-setofischemicstrokeinEHpatients.Amongmalepatients,pulsepressure,hsCRP,IMTandHDL-CwerehigherinpatientscarryingAallelethanBallele(P<0.05).Whilethesefactorsweredifferentinfemalepa-tientscarryingdifferentgenotypesinwhichAAallelewerehighest.Patientswithvariousgenotypesshoweddifferenturicacidlevelsbutshowednosignificantdifference.ConclusionAmongEHpatientswithcomplicatedischemicstroke,thosecarryingtheA/AAalleleshowhighlevelofriskfactorsandislikelytohavethesusceptibilityofrecurrenceofstroke.

简介：ObjectivesToinvestigateeffectofAngll,captoprilonsingleguineamyocytesonL-typecalciumcurrentandsodiumcurrent.MethodsMembranepatchclampwholecellrecordingtechniquewasusedtoinvestigateeffectofangll,captoprilonL-Camaximumcurrentdensityandsodiummaximumcurrentdensity.ResutlsAngllincreasedthemaximumcurrentdensitycomparedwithcontrolafterperfused5min,357.7±219.7Vs279.5±240.5PA/PF,increaserateis27.9%,theshapeofcurrent-voltagerelationshipcurvewasunchanged,peakedat+10mv,indicatedthatangllincreasedL-Cacurrentdensityinvoltage-dependent.Afterperfusedwithcaptopril,captopril+angll3,5min,L-Cacurrentwasrecorded,resultssuggestL-Camaximumcurrentdensitydecreasedsignificantlycomparedwithcontrol,incaptoprilgroup,128.4±92.6Vs286.2±89.7,66.7±68.3Vs286.2±89.7,respectively,rateofinhibitionis55.1%,76.6%,respectively.L-Cacurrentfurtherdecreasedincaptoprilpe

简介：BackgroundAngiotensinⅡtype1receptor(ATR1)/AngiotensinⅡtype2receptor(ATR2)usuallyinteractwitheachotherintheirexpressionandphysiologicalfunctions,andnitricoxide(NO)isalwaysinvolvedinATR1/ATR2regulationinvivo.Endothelialcellsplayacrucialroleinthemaintenanceofvascularfunctionandinthepreventionofcardiovasculardiseases.ObjectivesToinvestigatetheeffectsofangiotensinⅡ(AngⅡ)andATR1blockervalsartanonATR1,ATR2expressionandtheirrelationwithendothelialnitricoxidesynthase(eNOS)expression,andNOproductioninculturedvascularendothelialcells.MethodsHumanumbilicalveinendothelialcellline(HUVEC)andbovineaorticendothelialcell(BAEC)wereused.BAECwereisolatedfromaortaofnewborncalfbyenzymedigestionandcellsof3-5passageswereused.Cellswereincubatedwithvehicle,AngⅡ,valsartan,orAngⅡplusvalsartanrespectivelyforvariousperiods.ATR1,ATR2,eNOSexpressionandNOproductionweredetected.ResultsIncubationwithAngⅡorvalsartanapparentlydownregulatedATR1mRNAandproteinexpressioninvascularendothelialcells,andthecombinationeffectofthetwodrugsweremoreapparent.AngⅡshowedatransientslightlypromotiveeffectoneNOSandNOgenerationinBAECandanapparentlyinhibitoryeffectwithprolongedincubation,whilevalsartancanapparentlyreversethoseeffects.ConclusionsBothAngⅡandvalsartandownregulatedtheexpressionofATR1invascularendothelialcells.Thesynergisticeffectofthetwodrugswasmoreapparent.ProlongedincubationwithAngⅡcanapparentlyinhibiteNOSexpressionandNOproductioninendothelialcells,whilevalsartancanapparentlyreversethatinhibitoryeffect.

简介：AbstractBackground:Macrophages are involved in the pathogenesis of idiopathic pulmonary fibrosis, partially by activating lung fibroblasts. However, how macrophages communicate with lung fibroblasts is largely unexplored. Exosomes can mediate intercellular communication, whereas its role in lung fibrogenesis is unclear. Here we aim to investigate whether exosomes can mediate the crosstalk between macrophages and lung fibroblasts and subsequently induce fibrosis.Methods:In vivo, bleomycin (BLM)-induced lung fibrosis model was established and macrophages infiltration was examined. The effects of GW4869, an exosomes inhibitor, on lung fibrosis were assessed. Moreover, macrophage exosomes were injected into mice to observe its pro-fibrotic effects. In vitro, exosomes derived from angiotensin II (Ang II)-stimulated macrophages were collected. Then, lung fibroblasts were treated with the exosomes. Twenty-four hours later, protein levels of α-collagen I, angiotensin II type 1 receptor (AT1R), transforming growth factor-β (TGF-β), and phospho-Smad2/3 (p-Smad2/3) in lung fibroblasts were examined. The Student’s t test or analysis of variance were used for statistical analysis.Results:In vivo, BLM-treated mice showed enhanced infiltration of macrophages, increased fibrotic alterations, and higher levels of Ang II and AT1R. GW4869 attenuated BLM-induced pulmonary fibrosis. Mice with exosomes injection showed fibrotic features with higher levels of Ang II and AT1R, which was reversed by irbesartan. In vitro, we found that macrophages secreted a great number of exosomes. The exosomes were taken by fibroblasts and resulted in higher levels of AT1R (0.22 ± 0.02 vs. 0.07 ± 0.02, t = 8.66, P = 0.001), TGF-β (0.54 ± 0.05 vs. 0.09 ± 0.06, t= 10.00, P < 0.001), p-Smad2/3 (0.58 ± 0.06 vs. 0.07 ± 0.03, t= 12.86, P < 0.001) and α-collagen I (0.27 ± 0.02 vs. 0.16 ± 0.01, t = 7.01, P = 0.002), and increased Ang II secretion (62.27 ± 7.32 vs. 9.56 ± 1.68, t= 12.16, P < 0.001). Interestingly, Ang II increased the number of macrophage exosomes, and the protein levels of Alix (1.45 ± 0.15 vs. 1.00 ± 0.10, t = 4.32, P = 0.012), AT1R (4.05 ± 0.64 vs. 1.00 ± 0.09, t = 8.17, P = 0.001), and glyceraldehyde-3-phosphate dehydrogenase (2.13 ± 0.36 vs. 1.00 ± 0.10, t = 5.28, P = 0.006) were increased in exosomes secreted by the same number of macrophages, indicating a positive loop between Ang II and exosomes production.Conclusions:Exosomes mediate intercellular communication between macrophages and fibroblasts plays an important role in BLM-induced pulmonary fibrosis.

简介：高血压生产为与疾病联系的死亡经常负责的pathophysiological变化。overactive高血压蛋白原酶血管收缩素系统在高血压和与高血压联系的目标机关损坏的发展起一个中央作用，是明显的。我们以前发现了新奇血管收缩素受体(AT1)vaccine-ATR12181在自发地高血压的老鼠(SHR)稀释了高血压(BP)的发展人的必要高血压的模型。我们的目的是决定高BP的这变细是否与由高血压的状态导致的目标机关损坏的预防被联系。SHR被在联合复杂的peptide-tetanus-toxoid的重复下的注射与Freund的助手从AT1A受体的extracelluar部分对肽(编码ATR12181)使免疫。64个星期长期的观察被执行。重复种痘导致了anti-ATR12181抗体的正式就职。在观察的结束，种牛痘表明的SHR降低肾损害的BP，减少的心脏的肥大和变细。在心和肾的c-fos和c-jun的mRNA层次在种牛痘的SHR被减少。因为自我抗原被使用，疫苗的安全被担心。然而，自体免疫的疾病的符号没在心和肾的节被观察。这些数据证明对AT1受体的细胞外的部分的域的那重复免疫能对高血压引起一个目标机关保护。对AT1受体的活跃免疫可以在高血压的治疗被看作有希望的新策略。