-高血压英文课件Antihypert

AntihypertensiveDrugs

AntihypertensiveDrugs

1HypertensionHypertensionisnotadiseaseItisanarbitrarilydefineddisordertowhichbothenvironmentalandgeneticfactorscontributeMajorriskfactorfor:cerebrovasculardiseasemyocardialinfarctionheartfailureperipheralvasculardiseaserenalfailureHypertensionHypertensionisno2DefinitionElevationofarterialbloodpressureabove140/90mmHg.Canbecausedby:

anunderlyingdiseaseprocess:

In5-10%acausecanbefound (secondaryhypertension)

RenalarterystenosisHyperaldosteronismpheochromocytoma

idiopathicprocess(primaryoressentialhypertension)In95%ofcasesDefinitionElevationofarteria3Theleftventricleismarkedlythickenedinthispatientwithseverehypertensionthatwasuntreatedformanyyears.Themyocardialfibershaveundergonehypertrophy.Theleftventricleismarkedly4Thisleftventricleisverythickened(slightlyover2cminthickness),buttherestoftheheartisnotgreatlyenlarged.Thisistypicalforhypertensiveheartdisease.Thehypertensioncreatesagreaterpressureloadonthehearttoinducethehypertrophy.Thisleftventricleisveryth5MajorRiskFactorsThatIncreaseMortalityinHypertensionSmokingDyslipidemiasDiabetesMellitusAge>60Gender:men,postmenopausalwomenFamilyhistoryMajorRiskFactorsThatIncrea6PrevalenceThehypertensionprevalenceinthebigcities,smalltomediumcitiesandclass1toclass4ruralareasinChinawas20.4%,18.8%,21.0%,19.0%,20.2%and12.6%respectively

Pakistan(NHSP):theprevalenceofhypertensionis17.9%24%oftheUSAadultpopulationrepresenting43,186,000personshadhypertension.PrevalenceThehypertensionpr7Diagnosis

Diagnosisisgenerallybasedonrepeated,reproduciblemeasurementsofelevatedbloodpressureandnotonpatientsymptoms.Patientcomplianceisamajorobstacletotherapy

Diagnosis

Diagnosisisgeneral8StagesofHypertensionStageDiastolicRange(mmHg)SystolicRange(mmHg)HighNormal85-89130-139Stage190-99140-159Stage2100-109160-179Stage3>109>179StagesofHypertensionStageDia9TreatmentRationaleLong-termgoalofantihypertensivetherapy:Reducemortalityduetohypertension-induceddiseaseStrokeCongestiveheartfailureCoronaryarterydiseaseNephropathyPeripheralarterydiseaseRetinopathyTreatmentRationaleLong-termg10WaysofLoweringBloodPressureReducecardiacoutput(ß-blockers,Ca2+channelblockers)

Reduceplasmavolume(diuretics)

Reduceperipheralvascularresistance(vasodilators)MAP=COXTPRWaysofLoweringBloodPressur11"IndividualizedCare"RiskfactorsconsideredMonotherapyisinstitutedNonpharmacologicaltherapytriedfirstConsiderationsforchoiceofinitialmonotherapy: Reninstatus Coexistingcardiovascularconditions Otherconditions"IndividualizedCare"Riskf12HomeostasisofBloodPressureHomeostasisofBloodPressure13Determinantsofarterialpressure

BloodpressureiscontrolledbyanintegratedsystemPrimecontributorstobloodpressureare:CardiacoutputStrokevolumeHeartratePeripheralvascularresistanceAP=COxTPREachofthesefactorscanbemanipulatedbydrugtherapy

TreatmentofhypertensionseekstolowerCOand/orTPR.Determinantsofarterialpress14ForShort-TermNeuralControlBaroreceptorreflex

Sitorstandupquickly,BPfalls

neuralresponsesreestablishnormalBP

or

Suddenincreaseinstrokevolume,BPrises,neuralresponsesreestablishnormalBPForShort-TermNeuralControlB15

16Figure15-22Figure15-2217SympatheticnervouscontrolSympatheticnervouscontrol18Long-termRenalControlofBP:DirectPressureDiuresisBloodvolumetoohigh,Renal

Sympatheticvasoconstrictionreduced

Morefluidenterskidney,moreurineformedLowersBPvialowerbloodvolumeBloodpressuretoolow,Renal Sympatheticvasoconstrictionrises

Lessfluidenterskidney,lessurineformed

RaisesBPbyhigherbloodvolumeLong-termRenalControlofBP:19Figure15-9Figure15-920RenalControlofBP:IndirectIfBPtoolow,increaseBPbyincreasing__________Kidneycellssecrete_______

ConvertsangiotensinogentoangiotensinI

_______________________inlungconverts

angiotensinItoangiotensinII….RenalControlofBP:Indirect21Renin-angiotensinsystemRenin-angiotensinsystem22SummaryofLongTermRenalControlofBP RegulatesBPbyChanging:

1.

Directly–byallowingmoreorlessfluid toenterkidneytubulesIndirectly–Reabsorbingmorefluidthatwasalreadydestinedtobeurine2. Vasoconstriction/vasodilation SummaryofLongTermRenalCon23MAJORANTIHYPERTENSIVEDRUGS1)Diuretics

-Thiazidesandcongeners.-Loopdiuretics.-Potassium-sparingdiuretics.2)Sympatholyticdrugs-Centrallyactingantiadrenergicagents.-Adrenergicneuronblockingagents.-Alphaadrenergicblockers.-Betaadrenergicblockers.-Alpha-betaadrenergicblockers.3)Vasodilators-Nitricoxidereleasers.-Potassiumchannelopeners.-Calciumchannelblockers.4)Angiotensininhibitorsandantagonists.-AngiotensinConvertingEnzyme(ACE)inhibitors.-Angiotensinreceptorantagonists.MAJORANTIHYPERTENSIVEDRUGS1)24--高血压英文课件Antihypert25DiureticsFirst-linedrugLowdosediuretictherapyissafeandeffectiveinpreventingHTNcomplicationshydrochlorothiazide(Hydrodiuril),chlorthalidone(Hygrotonfurosemide

spironolactoneDiureticsFirst-linedrug26--高血压英文课件Antihypert271.ThiazidediureticsThiazidesarethemosteffectivediureticstoreducebloodpressureinpatientswithnormalrenalfunction.Theantihypertensivesdosesarelowerthatthoserequiredfordiureticeffect.MOA:Theinitialhypotensiveeffectsofdiureticsisassociatedwithareductioninbloodvolumeandcardiacoutput.Peripheralvascularresistanceisunaffected.1.ThiazidediureticsThiazides28After6-8weeksofcontinuoustherapyintravascularvolumeandcardiacoutputreturntowardsnormalwhileperipheralvascularresistancedecreases.

-MechanismsofthisdecreaseareprobablyrelatedtoadepletionofbodyNa+storeswhichleadsto:a)adecreaseofinterstitialfluidvolumeb)afallinsmoothmuscleNa+concentrationthatinturndecreasesintracellularCa++concentration

c)achangeinresponseofcellsurfacereceptorstovasoconstrictorhormones--高血压英文课件Antihypert29Thiazidediuretics:mechanismofactionCOThenThiazidediuretics:mechanism30EffectofthiazidesonBP:kineticEffectofthiazidesonBP:kin31Thiazidediuretics:clinicaluseUsedformonotherapyofmildhypertensionandforpolydrugtherapyofmoreseverecases.Therapeuticexpectationwithmonotherapy:20/10mmHgdropin60%ofpatients.Uselowdoses(ceilingeffect)tominimizeside-effects(Kloss).Low-dosethiazide/lowdosebeta-blockercomboCanbeusedinconjunctionwithsympatholytics,ACEI,Ca-channelblockersThiazidediuretics:clinicalu32ThiazideDiuretics:side-effects.MajorSide-effects:a)Kloss

(minimizedbyusinglowdoses,diet,useofcomboswithK-sparingdiuretics).b)hyperuricemia

(badforgout)c)hyperglycemia,glucoseintolerance(badfordiabetes)d)increaseLDL&VLDL(badforatherosclerosis)Beneficialeffect:Ca-sparing(goodforosteoporosis)ThiazideDiuretics:side-effec33FurosemideandhighceilingdiureticsUseinhypertensionislimited.OntheirowntheyarenotveryeffectiveatloweringBPMainindicationsare:a)severehypertensionwhenseveraldrugswithNa-retainingpropertiesareused(e.g.hydralazine,majorsympatholytics).Usuallyabeta-blockerisalsorequired.b)whenGFRis<30-40ml/minc)inCHForcirrhosis.Furosemideandhighceilingdi34Propranolol

Nadolol

"nonselective"Pindolol-"nonselective";

partialagonist(someintrinsicsympathomimeticactivity);lessbradycardiathanotherbeta-blockers

Metoprolol-beta1"selective"

Labetolol-""beta/alpha";

higherinstanceofsideeffects(orthostatichypotension;sexualdysfunction);usefulinhypertensionofpheochromocytomas

Beta-adrenergicantagonistsBeta-adrenergicantagonists35Beta-adrenergicantagonistsMechanismofaction:beta-1blockadea)inheart(theyreducecardiaccontractilityandCO).b)inkidney(theyreducereninreleasebysympatheticnerves).DropinAIIproduces:-Nalossbykidney(leadingtoBVreduction)-vascularrelaxationinsomevascularbeds.c)intheCNS(controversial)Beta-adrenergicantagonistsMec36Beta-blockers:mechanismofactioninhypertensionBeta-blockers:mechanismofac37Beta-adrenergicantagonists:side-effects/1Bronchoconstriction(minimizedbyusingbeta-1selectivedrug;badforasthmatics)IncreaseinLDL/HDLratio(badforatherosclerosis)Depression,lossofenergy(CNSeffect)IncreaseAVnoderefractoriness(goodforSVTsbutcouldbebadifabnormalSAorAVnodes)Decreasedcardiaccontractility(goodforangina,goodorbadforCHF)Beta-adrenergicantagonists:s38Beta-adrenergicantagonists:side-effects/2Blockprodromalsignsofhypoglycemiaininsulin-dependantdiabetics.Withdrawal:ReboundhypertensionandcardiacischemiaColdextremities.MayprecipitateorworsenRaynaud’sdisease(vasospasmofextremitiesduetobeta-blockadeofAVshunts).Labetatol(alpha+betablocker)orblockerwithISAmaybepreferedinthiscase.Adverseeffectinpatientswithocclusiveperipheralvasculardisease(Productionoraggravationofintermittentclaudication.ICisduetolowcalfbloodflow)Beta-adrenergicantagonists:s39Beta-blockers:clinicaluseinhypertensionCbinedwithlowdosethiazideShouldnotbecombinedwithverapamilordiltiazemtoavoidexcessivecardiacdepressionNon-selective,beta-1selectiveandblockerswithISAworkequallywell.CanbecombinedwithACEI,dihydropyridines(cautiously),othervasodilators.Beta-blockers:clinicalusein40Renin-angiotensinsystemRenin-angiotensinsystem41ACEinhibitors:mechanismofantihypertensiveactionACEIsAIIand

bradykinin(vasodilator).InthecontextofhypertensionACEIswork:bypreloadandafterloadvia:a)arteriolardilation(TPR). b)Nareabsorptionbykidney(hemodynamiceffectonkidneyanddropinaldosteronesecretion).Thisreducesbloodvolumeandpreloadc)releaseofNE(whichlowersTPRandCO)d)cardiaccontractilityACEinhibitors:mechanismofa42ACEIs:mechanismofactionACEIs:mechanismofaction43ACEIs:side-effects/druginteractionsSAFE,effectiveandwell-tolerated.Fewside-effectsbutsomepotentiallyserious.Commonside-effectsareduetobradykininaccumulation:cough,skinrashes,angioedemaHyperkalemia(badinpresenceofK-sparingdiuretic,goodinpresenceofthiazide)Firstdoseorthostatichypotension(canbesevereinhypovolemicpatiente.g.usingdiuretics)Riskofseverefoetalpbs.AcuteRenalfailureinpatientwithhighgraderenalarterystenosis.ACEIs:side-effects/druginter44UseofACEIsinhypertensionExcellentfirstlineagentformonotherapyinabsenceofrenalischemia.Canbecombinedwithbeta-blockersorthiazidesdiuretics(NOTwithK-sparingdiuretics)oralpha-1blockersforenhancedeffectiveness.Not

forpregnantwomen.OthermajorusesofACEIs:diabeticnephropathy,CHFandpostMItreatment.UseofACEIsinhypertensionEx45ACEIsdifferencesbetweenagentsLittledifferenceexcept:T1/2.a)short(2hrs)e.g.captoprilb)long(~10-12hrs)e.g.enalapril,linosipril,fosinopril,severalothers.Excretion:a)renal(mostdrugs).Dosesshouldbereducedinpatientswithrenalinsufficiency.b)somelivermetabolism(fosinopril)ACEIsdifferencesbetweenagen46AngiotensinreceptorantagonistsPrototype:Losartan.BlockAT1notAT2receptors,noeffectonbradykinin.LessefficaciousthanACEIs(??)Effectpotentiatedbythiazide.Producesneithercoughnorangiodema(bradykinineffects)butotherside-effectsarethesameasthoseofACEIs.Angiotensinreceptorantagonis47DifferencebetweenACEIs&AT1blockers

AngIIBradykinin

AT1-RAT2-RVasoconstriction

Vasorelaxation

AngIIBradykinin

AT1-R

AT-2RVasoconstrictionVasorelaxationACEIsAT1RantagonistsNormal

ReducedIncreasedDifferencebetweenACEIs&AT148DHPs:mechanismofactionSNAisminimalwithlong-lastingDHPsDHPs:mechanismofactionSNA49DihydropyridineCachannelblockersMechanismofantihypertensiveaction:arteriolarvasodilation,TPRdrop.DHPsareslightlymorepotentantihypertensivesthanverapamilordiltiazemSide-effects:a)orthostatichypotensionb)reflextachycardiamayleadtocardiacischemiaand/orarrhythmias(minimizedbyusingslow-onsetandlong-lastingpreps)c)headache,flushing,dizziness

d)pedaloedema.

DihydropyridineCachannelblo50Non-selectiveCachannelblockers:mechanismofactionNon-selectiveCachannelblock51Non-selectiveCachannelblockers:side-effectsSide-effects:

a)SAnodeinhibition:probablygoodasitpreventsthebaroreflexmediatedtachycardiab)increaseinAVnoderefractoriness.GoodforSVTsbutcanproduceAVblockinpatientswithcardiacconductionproblems.c)decreasecardiaccontractilityNon-selectiveCachannelblock52CentrallyActingDrugs

Clonidineactivatesalpha2andimidazolinereceptorsinthevasomotorcenterofthemedullawhichinhibitsthesympatheticnervoussystem.

Consideredasecond-linedrugorforspecialcases(iemethyldopainpregnanthypertensivepatients).Areducedheartrateandcardiacoutputaccountforreductioninbloodpressure.CentrallyActingDrugsClonidi53Alpha-2adrenergicagonistsClonidine,guanabenz,guanfacine,alpha-methyldopa(thelatterisaprodrugconvertedintoalpha-methylNE).Mechanismsofaction:sympatholytics;reduceCO&TPRa)Majorsite:CNS.Reduceactivityofsympatheticnervesbyactiononvasomotorcenterb)peripheralsite:reducereleaseofNEfromsympatheticterminalsAlpha-2adrenergicagonistsClo54CentrallyActingDrugs

AntihypertensiveeffectresultsfromactionintheCNScausingareducedsympatheticnervefiringrate.Prototype:clonidineCentrallyActingDrugsAntihyp55MechanismofactionofclonidinePeripheral

effectCentraleffectMechanismofactionofclonidi56Alpha-2adrenergicagonists:side-effectsSedationDepressionDrymouth,constipation.Reboundhypertension(clonidinebutnotalphamethyl-dopa)ImpairmentofsexualfunctionNaretention(improvedbyuseofdiuretics)Alpha-2adrenergicagonists:s57Alpha-2adrenergicagonists:therapeuticstatusSecond-linedrugsinhypertension,notusedformonotherapy.Useofslow-releasepatch(clonidine)improvesside-effects)Methyl-dopaissafeinpregnancy.Note:alpha-2adrenergicagonistsareusedtotreatglaucoma,pain,spasticityandopiatewithdrawal.Alpha-2adrenergicagonists:t58GanglionicblockersHistoricalinterestonly.Thesedrugsproduceintolerableside-effects(orthostasis,Naretention,GIandsexualdysfunction)trimethaphanwaswithdrawnin1996mecamylaminestillavailablebutneverused.GanglionicblockersHistorical59ReserpineDepletesNEfromstoragevesiclesMajoractionisinCNS.Reducessympatheticoutflow.Reasonablyeffective,especiallywiththiazide.Side-effects:depression,sedation,GIhyperactivity.Cheap,itsonlyvirtue.

Littleusedatpresent.ReserpineDepletesNEfromstor60GuanethidinePeripheralsympatholyticdrug.RidestheNEtransporter,dislodgesNEfromvesiclesandpreventsexocytosis.Lotsofside-effects:posturalhypotensioncerebralischemia,GIhyperactivity,sexualdysfunctionPotentiallyveryseriousdruginteractions(tricyclics,indirectlyactingsympathomimeticse.g.coldmedicines)Useinhypertensionrestrictedtoseverecases.MustbecombinedwithdiureticGuanethidinePeripheralsympath61Vasodilators:Hydralazine&Minoxidil

Oralvasodilatorsusedareusedforlong-termoutpatienttreatmentofseverehypertensioninthecontextofapolydrugtherapy.Workbyreducingafterload(TPR).CausemarkedNaretentionandrapidlyincreaseBV(pseudotolerance)i.e.mustbeusedinconjunctionwithdiuretics.Causemarkedreflextachycardiaandincreasedcontractility(beta-mediated)ergomustbeusedwithbeta-blockers.Minoxidilcauseshypertrichosis(growthofbodyhair).Vasodilators:Hydralazine&Min62Alpha-1adrenergicantagonistsMechanismofaction:

a)antagonizeeffectofsympathetictoneinarteriesandveins(reduceTPRandpreload)b)reducebaroreflexviacentralaction(thusproduceverylittlereflextachycardia).Side-effects:few

a)first-dosehypotension(Pbwitholderpatients)b)retentionofsaltandwaterAlpha-1adrenergicantagonists63Alpha1-blockers:mechanismofactionAlpha1-blockers:mechanismof64Alpha-1adrenergicantagonists:therapeuticuseCanbeusedformonotherapyofmildhypertensionMayimproveLDL/HDLratioEffectsadditivewiththiazidediureticsandACEI.Shouldnotbecombinedwithvasodilators(e.g.dihydropyridines):tachycardia.Goodforpatientswithbenignprostatichyperplasia.Alpha-1adrenergicantagonists65Alpha-1adrenergicantagonists:differencebetweenagentsPrototype:prazosinNeweragents(terazosin,doxazosin)havelongerT1/2.Neweragentscanbegivenonceaday.Alpha-1adrenergicantagonists66TreatmentofmildhypertensionNonpharmacological(saltrestriction,exercise,weightloss)Pharmacological:alternativesforinitialtreatmentinclude:a)monotherapywiththiazide,ACEI,beta-blockeroralpha-1blockerorcalcium-channelblocker.Drugisselectedonthebasisofefficacy,concurrentpathologiesandindividualsensitivitytoside-effects.b)lowthiazide/lowbeta-blockercomboc)thiazide/Ksparingcombo.Treatmentofmildhypertensio67PrinciplesofpolydrugtherapyMonotherapyissufficientinonly55%ofcases.

Inmoreseverecases2or3drugshavetobeused.EachdrugmustbelongtoadifferentclassThecombinationof2first-linedrugsistriedfirst.OneofthedrugsislikelytobeanACEI.Vasodilatorsifusedmustbegivenwithadiureticandabeta-blocker.Principlesofpolydrugtherapy68TreatmentofhypertensiveemergenciesGoal:producearapidbutwellcontrolledfallinBP.Context:hypertensiveencephalopathy,eclampsia,pheo,hypertensionwithpulmonaryoedema,aneurism,subarachnoidhemorrhageetc..Labetaloliv(alpha&betablocker)I.vnitroprussideI.v.nitroglycerinehydralazineivorim(eclampsia)ivphentolamineorphenoxybenzaminepo(pheo)Treatmentofhypertensiveemer69AntihypertensiveDrugs

AntihypertensiveDrugs

70HypertensionHypertensionisnotadiseaseItisanarbitrarilydefineddisordertowhichbothenvironmentalandgeneticfactorscontributeMajorriskfactorfor:cerebrovasculardiseasemyocardialinfarctionheartfailureperipheralvasculardiseaserenalfailureHypertensionHypertensionisno71DefinitionElevationofarterialbloodpressureabove140/90mmHg.Canbecausedby:

anunderlyingdiseaseprocess:

In5-10%acausecanbefound (secondaryhypertension)

RenalarterystenosisHyperaldosteronismpheochromocytoma

idiopathicprocess(primaryoressentialhypertension)In95%ofcasesDefinitionElevationofarteria72Theleftventricleismarkedlythickenedinthispatientwithseverehypertensionthatwasuntreatedformanyyears.Themyocardialfibershaveundergonehypertrophy.Theleftventricleismarkedly73Thisleftventricleisverythickened(slightlyover2cminthickness),buttherestoftheheartisnotgreatlyenlarged.Thisistypicalforhypertensiveheartdisease.Thehypertensioncreatesagreaterpressureloadonthehearttoinducethehypertrophy.Thisleftventricleisveryth74MajorRiskFactorsThatIncreaseMortalityinHypertensionSmokingDyslipidemiasDiabetesMellitusAge>60Gender:men,postmenopausalwomenFamilyhistoryMajorRiskFactorsThatIncrea75PrevalenceThehypertensionprevalenceinthebigcities,smalltomediumcitiesandclass1toclass4ruralareasinChinawas20.4%,18.8%,21.0%,19.0%,20.2%and12.6%respectively

Pakistan(NHSP):theprevalenceofhypertensionis17.9%24%oftheUSAadultpopulationrepresenting43,186,000personshadhypertension.PrevalenceThehypertensionpr76Diagnosis

Diagnosisisgenerallybasedonrepeated,reproduciblemeasurementsofelevatedbloodpressureandnotonpatientsymptoms.Patientcomplianceisamajorobstacletotherapy

Diagnosis

Diagnosisisgeneral77StagesofHypertensionStageDiastolicRange(mmHg)SystolicRange(mmHg)HighNormal85-89130-139Stage190-99140-159Stage2100-109160-179Stage3>109>179StagesofHypertensionStageDia78TreatmentRationaleLong-termgoalofantihypertensivetherapy:Reducemortalityduetohypertension-induceddiseaseStrokeCongestiveheartfailureCoronaryarterydiseaseNephropathyPeripheralarterydiseaseRetinopathyTreatmentRationaleLong-termg79WaysofLoweringBloodPressureReducecardiacoutput(ß-blockers,Ca2+channelblockers)

Reduceplasmavolume(diuretics)

Reduceperipheralvascularresistance(vasodilators)MAP=COXTPRWaysofLoweringBloodPressur80"IndividualizedCare"RiskfactorsconsideredMonotherapyisinstitutedNonpharmacologicaltherapytriedfirstConsiderationsforchoiceofinitialmonotherapy: Reninstatus Coexistingcardiovascularconditions Otherconditions"IndividualizedCare"Riskf81HomeostasisofBloodPressureHomeostasisofBloodPressure82Determinantsofarterialpressure

BloodpressureiscontrolledbyanintegratedsystemPrimecontributorstobloodpressureare:CardiacoutputStrokevolumeHeartratePeripheralvascularresistanceAP=COxTPREachofthesefactorscanbemanipulatedbydrugtherapy

TreatmentofhypertensionseekstolowerCOand/orTPR.Determinantsofarterialpress83ForShort-TermNeuralControlBaroreceptorreflex

Sitorstandupquickly,BPfalls

neuralresponsesreestablishnormalBP

or

Suddenincreaseinstrokevolume,BPrises,neuralresponsesreestablishnormalBPForShort-TermNeuralControlB84

85Figure15-22Figure15-2286SympatheticnervouscontrolSympatheticnervouscontrol87Long-termRenalControlofBP:DirectPressureDiuresisBloodvolumetoohigh,Renal

Sympatheticvasoconstrictionreduced

Morefluidenterskidney,moreurineformedLowersBPvialowerbloodvolumeBloodpressuretoolow,Renal Sympatheticvasoconstrictionrises

Lessfluidenterskidney,lessurineformed

RaisesBPbyhigherbloodvolumeLong-termRenalControlofBP:88Figure15-9Figure15-989RenalControlofBP:IndirectIfBPtoolow,increaseBPbyincreasing__________Kidneycellssecrete_______

ConvertsangiotensinogentoangiotensinI

_______________________inlungconverts

angiotensinItoangiotensinII….RenalControlofBP:Indirect90Renin-angiotensinsystemRenin-angiotensinsystem91SummaryofLongTermRenalControlofBP RegulatesBPbyChanging:

1.

Directly–byallowingmoreorlessfluid toenterkidneytubulesIndirectly–Reabsorbingmorefluidthatwasalreadydestinedtobeurine2. Vasoconstriction/vasodilation SummaryofLongTermRenalCon92MAJORANTIHYPERTENSIVEDRUGS1)Diuretics

-Thiazidesandcongeners.-Loopdiuretics.-Potassium-sparingdiuretics.2)Sympatholyticdrugs-Centrallyactingantiadrenergicagents.-Adrenergicneuronblockingagents.-Alphaadrenergicblockers.-Betaadrenergicblockers.-Alpha-betaadrenergicblockers.3)Vasodilators-Nitricoxidereleasers.-Potassiumchannelopeners.-Calciumchannelblockers.4)Angiotensininhibitorsandantagonists.-AngiotensinConvertingEnzyme(ACE)inhibitors.-Angiotensinreceptorantagonists.MAJORANTIHYPERTENSIVEDRUGS1)93--高血压英文课件Antihypert94DiureticsFirst-linedrugLowdosediuretictherapyissafeandeffectiveinpreventingHTNcomplicationshydrochlorothiazide(Hydrodiuril),chlorthalidone(Hygrotonfurosemide

spironolactoneDiureticsFirst-linedrug95--高血压英文课件Antihypert961.ThiazidediureticsThiazidesarethemosteffectivediureticstoreducebloodpressureinpatientswithnormalrenalfunction.Theantihypertensivesdosesarelowerthatthoserequiredfordiureticeffect.MOA:Theinitialhypotensiveeffectsofdiureticsisassociatedwithareductioninbloodvolumeandcardiacoutput.Peripheralvas