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Medchemexpress/Angiotensin 1-7(Synonyms: Angiotensin-(1-7); Ang-(1-7))/HY-12403/10mM*1mL in Water
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Medchemexpress/Angiotensin 1-7(Synonyms: Angiotensin-(1-7); Ang-(1-7))/HY-12403/10mM*1mL in Water
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Angiotensin(1-7)inhibitspurifiedcanineangiotensinconvertingenzyme(ACE)activitywithanIC50of0.65μM.
Description

Angiotensin(1-7)inhibitspurifiedcanineangiotensinconvertingenzyme(ACE)activitywithanIC50of0.65μM.

IC50&Target

IC50:0.65μM(ACE)[1]

InVitro

Angiotensin1-7(Ang1-7)actsasalocalsynergisticmodulatorofkinin-inducedvasodilationbyinhibitingACEandreleasingnitricoxide(NO).Angiotensin(1-7)augmentsthevasodilationinducedbybradykinin(BK)inaconcentration-dependentmannerinringspreconstrictedwiththethromboxaneanalogU46619.TheEC50ofBK(2.45±0.51nMversus0.37±0.08nM)isshiftedleftwardby6.6-foldinthepresenceof2μMconcentrationofAngiotensin(1-7).TheBK-inducedrelaxationresponseisaugmentedbyAngiotensin(1-7)(0.1to2μM)inadose-dependentmanner.Ataconcentrationof2μMAngiotensin(1-7),relaxationtoBKisincreased92%comparedtoBKalone(41±4.4%versus92±2.5%,P<0.01). angiotensin="" (1-7)="" possesses="" novel="" biological="" functions="" that="" are="" distinct="" from="" ang="" ii.="" in="" contrast="" to="" ang="" ii,="" angiotensin="" (1-7)="" is="" not="" a="" dipsogen="" or="" an="" aldosterone="" secretagogue,="" but="" similar="" to="" ang="" ii,="" it="" stimulates="" the="" release="" of="" vasopressin,="" prostaglandins,="" and="" no.="" angiotensin="" (1-7)="" counteracts="" several="" actions="" of="" ang="" ii.="" in="" both="" canine="" and="" porcine="" coronary="" arteries,="" angiotensin="" (1-7)="" causes="" vasodilation,="" while="" ang="" ii="" divergently="" constricts="" the="" coronary="" arteries.="" angiotensin="" (1-7)="" inhibits="" cultured="" vascular="" smooth="" muscle="" cell="" growth,="" whereas="" equal="" molar="" concentration="" of="" ang="" ii="" stimulates="" cell="">[1].Angiotensin1-7(Ang1-7)abrogatesthemethylglyoxal-modifiedalbumin(MGA)-stimulatedmyofibroblastphenotypebyinhibitingthechronicstimulationoftheTGF-β-ERKpathwayinNRK-52Ecells[2].

InVivo

AsevenfolddecreaseintheplasmalevelofAngiotensin1-7(Ang1-7)isdemonstratedindextransulfatesodium(DSS)treatedmicecomparetountreated(UT)groupatday7postcolitisinduction.Ontheotherhand,asignificantincreaseinAng1-7isobservedincolonhomogenatesofDSStreatedmiceatday7(0.09ng/mL)comparetoUTmice(0.04ng/mL)[3].Theovariectomized(OV)femaleWistar-ratsreceiveestrADIol(500μg/kg/week)orvehiclefortwoweeks.Theanimalsareanesthetized,cannulated,andtheresponsesincludingmeanarterialpressure,renalbloodflow(RBF),andrenalvascularresistanceattheconstantlevelofrenalperfusionpressuretogradedinfusionofAngiotensin1-7(Ang1-7)at0,100and300ng/kg/minaredeterminedinOVandOVestradiol-treated(OVE)rats,treatedwithvehicleorMasRantagoNIST;A779.RBFresponsetoAng1-7infusionincreaseddose-dependentlyinvehicle(Pdose<0.001) and="" a779-treated="">dose<0.01) animals.="" however,="" when="" masr="" is="" blocked,="" the="" rbf="" response="" to="" ang="" 1-7="" significantly="" increases="" in="" ov="" animals="" compare="" with="" ove="" rats=""><0.05). when="" estradiol="" is="" limited="" by="" ovariectomy,="" a779="" increases="" rbf="" response="" to="" angiotensin="" (1-7)="" administration,="" while="" this="" response="" is="" attenuated="" in="" ove="">[4].

References

  • [1].LiP,etal.Angiotensin-(1-7)augmentsbradykinin-inducedvasodilationbycompetingwithACEandreleasingnitricoxide.Hypertension.1997Jan;29(1Pt2):394-400.

    [2].AlzayadnehEM,etal.Angiotensin-(1-7)abolishesAGE-inducedcellularhypertrophyandmyofibroblasttransformationviainhibitionofERK1/2.CellSignal.2014Sep19.pii:S0898-6568(14)00314-3.

    [3].KhajahMA,etal.Anti-InflammatoryActionofAngiotensin1-7inExperimentalColitis.PLoSOne.2016Mar10;11(3):e0150861.

    [4].SaberiS,etal.RoleofMasreceptorinrenalbloodflowresponsetoangiotensin-(1-7)inovariectomizedestradioltreatedrats.ResPharmSci.2016Jan-Feb;11(1):65-72.

KinaseAssay
[1]

CompetitionassaysusingpurifiedcanineACEaredeterminedusingafixedconcentrationofthesubstrateHip-His-Leu(1mM)andvaryingtheconcentrationsofthecompetingagents[Lisinopril(0.1to100nM),Angiotensin(1-7)(10nMto10μM),orSar1,Thr8-AngII(10nMto10μM)].Inhibitoryconstants(IC50)aredeterminedfromtherespectivecompetitioncurves.TostudytheeffectofAngiotensin(1-7)onBKmetabolisminintactcoronaryrings,125I-[Tyr0]-BK(finalconcentrationof1nM)isaddedtothetubescontainingthreeringspreincubatedwith1mLKrebs"bufferandaeratedwith95%O2and5%CO2at37°C.Lisinopril(2μM),Angiotensin(1-7)(2μM),orKrebs"bufferascontrolareaddedtotherings10minutesbeforeadditionoftheradiolabeledBK.Aliquotsoftheincubationmediumareremovedat5,10,and20minutesanddilutedwith1%HFBAtoinhibitpeptidaseactivity[1].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

CellAssay
[2]

Angiotensin1-7(Ang1-7)ispreparedinsaline[2].

500μMMethylglyoxalisincubatedwith100μMBSAdissolvedinphosphatebufferedsaline(PBS)for24hours,thenwashedon10kDafilterstoremoveexcessmethylglyoxal,reconstitutedwithDMEM/F12serumfreemediaandpassedthrougha0.2μmicronfilter.TGF-β(5ng/mL)ispreparedtotreatcellsinasubsetofexperiments.Cellsareco-treatedwithoneorcombinationsofthefollowing:Angiotensin(1-7)(100nM),D-Ala7-Ang-(1-7)(10μM),ERK1/2kinaseinhibitor,PD98059(1μM),TGF-βreceptorkinaseinhibitor;SB525334(1μM),theAT1receptorantagonistLosartan(1μM),therenininhibitorAliskerin(1μM)andtheACEinhibitorLisinopril(1μM)[2].MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

AnimalAdministration
[3][4]

Angiotensin1-7(Ang1-7)isdissolvedin0.9%saline(MiceandRat)[3][4].

Mice[3]
MaleandfemaleBALB/cmice(1:1ratio,6-10weeksold,meanweight20g.)areused.Angiotensinfragment1-7acetatesalthydrate(Ang1-7)isdissolvedin0.9%saline(vehicle)at1mg/mLandstoredat-80°C.Variousdoses(0.01,0.06,0.1,0.3and1mg/kg)arefreshlypreparedfromthestockeachdayoftheexperiment,andadministeredtomicebydailyintra-peritoneal(i.p)injectionsinavolumeof500μLperinjection,eitherbefore(prophylacticapproach)orafter(treatmentapproach)DSStreatment.A779(MAS-1Rantagonist)issimilarlydissolvedindistilledwaterat1mg/mLandstoredat-80°C.Afreshlyprepareddoseof1mg/kgisadministeredtoasecondgroupofmicebydailyi.pinjectionsinavolumeof500μLdaily(for4days)alongwithcolitisinduction(prophylacticapproach).AthirdgroupofmicereceiveDSScontainingwateranddailyi.pinjectionsof0.9%saline(vehicle).ThefourthgroupreceiveDSScontainingwateralongwithdailyi.pinjectionswithDexamethasone(DEX)atdosesof0.01-1.0mg/kgoritsvehicle(0.9%saline)(prophylacticapproach).
Rat[4]
TwentysixovariectomizedfemaleWistarratsweighing200±20gareused.Angiotensin(1-7)isadministeredintravenouslybyamicrosyringepumpattwodifferentcontinuousdosesof100and300ng/kg/minafterantagonist/salineinfusion.Eachdoseisinfusedfor15min;andMAP,RPP,andRBFarerecordedduringAngiotensin(1-7)infusionandthelast3-5minofeachdosemeasuredas“responsetoAngiotensin(1-7)infusion”.DuringAngiotensin(1-7)infusion,RPPissustainedatpre-Ang1-7infusionlevelsviaanadjustableaorticclamp.Attheendoftheexperiment,theratsarehumanelykilledbyanestheticoverdose,andtheleftkidneysareremovedandweighedimmediately.MCEhasnotindependentlyconfirmedtheaccuracyofthesemethods.Theyareforreferenceonly.

References

  • [1].LiP,etal.Angiotensin-(1-7)augmentsbradykinin-inducedvasodilationbycompetingwithACEandreleasingnitricoxide.Hypertension.1997Jan;29(1Pt2):394-400.

    [2].AlzayadnehEM,etal.Angiotensin-(1-7)abolishesAGE-inducedcellularhypertrophyandmyofibroblasttransformationviainhibitionofERK1/2.CellSignal.2014Sep19.pii:S0898-6568(14)00314-3.

    [3].KhajahMA,etal.Anti-InflammatoryActionofAngiotensin1-7inExperimentalColitis.PLoSOne.2016Mar10;11(3):e0150861.

    [4].SaberiS,etal.RoleofMasreceptorinrenalbloodflowresponsetoangiotensin-(1-7)inovariectomizedestradioltreatedrats.ResPharmSci.2016Jan-Feb;11(1):65-72.

MolecularWeight

899.0

Formula

C₄₁H₆₂N₁₂O₁₁

CASNo.

51833-78-4

Storage
Powder-80°C2years
 -20°C1year
Insolvent-80°C6months
 -20°C1month
Shipping

RoomtemperatureincontinentalUS;mayvaryelsewhere

Solvent&Solubility

H2O:≥30.2mg/mL

*"<1 mg/ml"="" means="" slightly="" soluble="" or="" insoluble.="" "≥"="" means="" soluble,="" but="" saturation="">

Purity:98.62%

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