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potassium and hypertension

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Official reprint from UpToDate www.uptodate.com ©2015 UpToDate Authors Norman M Kaplan, MD David B Mount, MD Section Editor George L Bakris, MD Deputy Editor John P Forman, MD, MSc Potassium and hypertension All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Mar 2015. | This topic last updated: Nov 26, 2013. INTRODUCTION — A low dietary intake of potassium may increase the blood pressure, and potassium supplementation almost always lowers elevated blood pressure. The data demonstrating these associations, as well as the potential mechanisms, will be reviewed here. The approach to patients who present with concurrent hypertension and hypokalemia, and the clinical features of primary aldosteronism are discussed separately. (See "Approach to the patient with hypertension and hypokalemia" and "Pathophysiology and clinical features of primary aldosteronism" .) POTASSIUM INTAKE AND BLOOD PRESSURE — The level of potassium intake can affect blood pressure. The effect varies with the direction (low potassium intake raises the blood pressure and high potassium intake lowers the blood pressure) and magnitude of change in potassium intake. Lowpotassium diet — Low dietary potassium intake (below 40 meq/day [1.5 g/day]) has been associated with an elevation in blood pressure and an increased risk of stroke [1,2 ]. The following observations illustrate the range of findings: In addition to the adverse effects of low dietary potassium intake, the ratio of dietary sodium–topotassium intake can also influence blood pressure. In a report from the Dallas Heart Study, each threeunit increase in the urine sodiumtopotassium ratio, which can reflect increased sodium intake and/or reduced potassium intake, was associated with a 1.6/1 mmHg elevation in blood pressure [5 ]. Highpotassium diet — In contrast to the rise in blood pressure associated with a lowpotassium diet, potassium supplementation lowers the blood pressure significantly in hypertensive patients and insignificantly in normotensive patients. The magnitude of change was illustrated in a systematic review that included meta analyses of both randomized trials and cohort studies [6 ]. The following findings were noted: In another metaanalysis, the effect of potassium supplementation on blood pressure was greater in blacks ® ® In two different studies, one in healthy normotensive men [3 ] and one in patients with primary hypertension (formerly called essential hypertension) [4 ], potassium restriction from a normal intake of 80 to 90 meq/day down to 10 to 18 meq/day led to a statistically significant 4 to 5 mmHg increase in systolic blood pressure. The increase in blood pressure may have been mediated in part by sodium retention. ● In a prospective cohort study, individuals with a low dietary potassium intake (less than 64 meq/day [2.4 g/day]) had a 50 percent increase in the risk of stroke, independent of other risk factors such as the systemic blood pressure and diuretic therapy [2 ]. Similar findings were noted in a retrospective analysis of 28,880 patients at increased cardiovascular risk in two randomized trials [1 ]. At a median followup of 56 months, the risk of stroke was highest in patients with 24hour urine potassium excretion less than 40 meq/day (6.2 percent) and fell progressively at higher rates of 24hour urine potassium excretion to a low of 3.5 percent at more than 80 meq/day. ● In the metaanalysis of 16 randomized trials in hypertensive patients, increased potassium intake significantly reduced systolic blood pressure by a mean of 5.3/3.1 mmHg. In contrast, the reduction in systolic blood pressure was small (0.1/0.6 mmHg) and not statistically significant in three trials in normotensive subjects. ● When a subgroup analysis was performed according to achieved potassium intake, patients with an increase to 90 to 120 meq/day had the largest reduction in blood pressure (7.2/4.1 mmHg). ●

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  • 19/4/2015 Potassiumandhypertension

    http://www.uptodate.com/contents/potassiumandhypertension?topicKey=NEPH%2F3876&elapsedTimeMs=0&source=search_result&searchTerm=pota 1/5

    OfficialreprintfromUpToDate www.uptodate.com2015UpToDate

    AuthorsNormanMKaplan,MDDavidBMount,MD

    SectionEditorGeorgeLBakris,MD

    DeputyEditorJohnPForman,MD,MSc

    Potassiumandhypertension

    Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.Literaturereviewcurrentthrough:Mar2015.|Thistopiclastupdated:Nov26,2013.

    INTRODUCTIONAlowdietaryintakeofpotassiummayincreasethebloodpressure,andpotassiumsupplementationalmostalwayslowerselevatedbloodpressure.Thedatademonstratingtheseassociations,aswellasthepotentialmechanisms,willbereviewedhere.Theapproachtopatientswhopresentwithconcurrenthypertensionandhypokalemia,andtheclinicalfeaturesofprimaryaldosteronismarediscussedseparately.(See"Approachtothepatientwithhypertensionandhypokalemia"and"Pathophysiologyandclinicalfeaturesofprimaryaldosteronism".)

    POTASSIUMINTAKEANDBLOODPRESSUREThelevelofpotassiumintakecanaffectbloodpressure.Theeffectvarieswiththedirection(lowpotassiumintakeraisesthebloodpressureandhighpotassiumintakelowersthebloodpressure)andmagnitudeofchangeinpotassiumintake.

    LowpotassiumdietLowdietarypotassiumintake(below40meq/day[1.5g/day])hasbeenassociatedwithanelevationinbloodpressureandanincreasedriskofstroke[1,2].Thefollowingobservationsillustratetherangeoffindings:

    Inadditiontotheadverseeffectsoflowdietarypotassiumintake,theratioofdietarysodiumtopotassiumintakecanalsoinfluencebloodpressure.InareportfromtheDallasHeartStudy,eachthreeunitincreaseintheurinesodiumtopotassiumratio,whichcanreflectincreasedsodiumintakeand/orreducedpotassiumintake,wasassociatedwitha1.6/1mmHgelevationinbloodpressure[5].

    HighpotassiumdietIncontrasttotheriseinbloodpressureassociatedwithalowpotassiumdiet,potassiumsupplementationlowersthebloodpressuresignificantlyinhypertensivepatientsandinsignificantlyinnormotensivepatients.Themagnitudeofchangewasillustratedinasystematicreviewthatincludedmetaanalysesofbothrandomizedtrialsandcohortstudies[6].Thefollowingfindingswerenoted:

    Inanothermetaanalysis,theeffectofpotassiumsupplementationonbloodpressurewasgreaterinblacks

    Intwodifferentstudies,oneinhealthynormotensivemen[3]andoneinpatientswithprimaryhypertension(formerlycalledessentialhypertension)[4],potassiumrestrictionfromanormalintakeof80to90meq/daydownto10to18meq/dayledtoastatisticallysignificant4to5mmHgincreaseinsystolicbloodpressure.Theincreaseinbloodpressuremayhavebeenmediatedinpartbysodiumretention.

    Inaprospectivecohortstudy,individualswithalowdietarypotassiumintake(lessthan64meq/day[2.4g/day])hada50percentincreaseintheriskofstroke,independentofotherriskfactorssuchasthesystemicbloodpressureanddiuretictherapy[2].

    Similarfindingswerenotedinaretrospectiveanalysisof28,880patientsatincreasedcardiovascularriskintworandomizedtrials[1].Atamedianfollowupof56months,theriskofstrokewashighestinpatientswith24hoururinepotassiumexcretionlessthan40meq/day(6.2percent)andfellprogressivelyathigherratesof24hoururinepotassiumexcretiontoalowof3.5percentatmorethan80meq/day.

    Inthemetaanalysisof16randomizedtrialsinhypertensivepatients,increasedpotassiumintakesignificantlyreducedsystolicbloodpressurebyameanof5.3/3.1mmHg.Incontrast,thereductioninsystolicbloodpressurewassmall(0.1/0.6mmHg)andnotstatisticallysignificantinthreetrialsinnormotensivesubjects.

    Whenasubgroupanalysiswasperformedaccordingtoachievedpotassiumintake,patientswithanincreaseto90to120meq/dayhadthelargestreductioninbloodpressure(7.2/4.1mmHg).

  • 19/4/2015 Potassiumandhypertension

    http://www.uptodate.com/contents/potassiumandhypertension?topicKey=NEPH%2F3876&elapsedTimeMs=0&source=search_result&searchTerm=pota 2/5

    thaninwhites[7].Urinarypotassiumexcretioninblacksisconsistentlylessthaninwhites[8,9].Thisdifferenceisdueinparttolessdietarypotassiumintakeinblacks[9,10].

    Inadditiontothelowerrateofpotassiumintake,anotherfactorthatmaycontributetotheincreasedpredispositiontohypertensioninblacksisarelativeincreaseintheactivityoftheNaK2ClcotransporterintheluminalmembraneinthethickascendinglimboftheloopofHenleandthemaculadensa(figure1)[8].Thisdefectcouldcontributetothedecreasedplasmareninactivity,lowerrateofurinarypotassiumexcretion,andincreasedsaltsensitivityoftenseeninblacks.

    ClinicalimplicationsBasedupontheaboveobservations,ithasbeenproposedthathypertensivepatientswithnormalornearnormalrenalfunctionshouldbeencouragedtomaintainahighpotassiumintakefromfreshfruitsandvegetables[11].Dietarycounselingistheusualapproachtoincreasingpotassiumintake.

    Potassiumchloridesupplementscanalsobeused,particularlyiftheserumpotassiumconcentrationislow.However,ifthereisnoapparentcauseforthehypokalemia(eg,diuretictherapy,gastrointestinallosses),thepatientshouldbeevaluatedforthedisordersthatareassociatedwithbothhypertensionandhypokalemia.Theseincludeprimaryaldosteronism,renovasculardisease,andCushing'ssyndrome.(See"Approachtothepatientwithhypertensionandhypokalemia"and"Causesofhypokalemiainadults",sectionon'Diuretics'.)

    FewAmericansachievetherecommendedlevelofpotassiumintake.InareportfromtheNationalHealthandNutritionExaminationSurvey(NHANES)III,theaveragedailypotassiumintakeinadultswas74to82meq(2.9to3.2g)inmenand54to59meq(2.1to2.3g)inwomen[12].Only10percentofmenandlessthan1percentofwomenhadadailypotassiumintakeof120meq(4.7g)ormore.

    Wedonotrecommendpotassiumsupplementationorahighpotassiumdiettoattainthesegoalsinpatientsatriskforhyperkalemiadue,forexample,totherapywithangiotensininhibitors,potassiumsparingdiuretics,orunderlyingchronickidneydisease.

    MECHANISMSThemechanismsbywhichpotassiumintakemightberelatedtohypertensionandvasculardiseasearenotwelldefined.Thereductioninbloodpressurewithpotassiumsupplementsmayberelatedtodecreasedvascularresponsivenesstovasopressors,particularlynorepinephrine[13].Inaddition,sodiumandchlorideintakemaybeimportant.

    RelationtosodiumexcretionTherelationshipbetweenpotassiumandbloodpressureappearstobedueinparttochangesinsodiumexcretion,asnotedabove[5].Sodiumexcretionisdiminishedbyhypokalemiaoralowpotassiumdietandincreasedwithpotassiumsupplements,apparentlythroughchangesinsodiumreabsorptionintheproximaltubuleand/orloopofHenle[14].(See'Potassiumintakeandbloodpressure'aboveand"Hypokalemiainducedrenaldysfunction",sectionon'Increasedsodiumreabsorption'.)

    RoleofchlorideintakeChlorideisanimportantdeterminantoftheriseinbloodpressureinsaltsensitiveformsofhypertension.Incomparison,dietarypotassium(eg,fromfruitsandvegetables)isprimarilyassociatedwithorganicanionssuchascitrate,notchloride.(See"Saltintake,saltrestriction,andprimary(essential)hypertension".)

    Therelativeefficacyofpotassiumbicarbonateorpotassiumcitrate(citrateismetabolizedtobicarbonate)supplementsandpotassiumchloridesupplementshasbeendirectlyevaluatedinrandomizedcrossovertrialsofpatientswithhypertension[15,16].Thebicarbonate,citrate,andchloridepreparationallproducedasimilarreductioninbloodpressure.Thus,theavailableevidencedoesnotsupporttheaccompanyinganionbeingimportantintheeffectofpotassiumonbloodpressure.

    SUMMARY

    Maintenanceofadequatepotassiumintakeortheadministrationofpotassiumsupplementsusuallylowersthebloodpressure,particularlyinblacksandinpatientswhoarenotsodiumrestricted.Furthermore,ahigherpotassiumintakereducestheriskofstroke.(See'Potassiumintakeandbloodpressure'aboveand'Relationtosodiumexcretion'above.)

    Themechanismbywhichpotassiumreducesbloodpressureisnotclear.(See'Mechanisms'above.)

    Someexpertssuggestthathypertensivepatientsshouldconsumeatleast120meq(4.7g)ofdietary

  • 19/4/2015 Potassiumandhypertension

    http://www.uptodate.com/contents/potassiumandhypertension?topicKey=NEPH%2F3876&elapsedTimeMs=0&source=search_result&searchTerm=pota 3/5

    UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.

    REFERENCES

    1. O'DonnellMJ,YusufS,MenteA,etal.Urinarysodiumandpotassiumexcretionandriskofcardiovascularevents.JAMA2011306:2229.

    2. GreenDM,RopperAH,KronmalRA,etal.Serumpotassiumlevelanddietarypotassiumintakeasriskfactorsforstroke.Neurology200259:314.

    3. KrishnaGG,MillerE,KapoorS.Increasedbloodpressureduringpotassiumdepletioninnormotensivemen.NEnglJMed1989320:1177.

    4. CoruzziP,BrambillaL,BrambillaV,etal.Potassiumdepletionandsaltsensitivityinessentialhypertension.JClinEndocrinolMetab200186:2857.

    5. HedayatiSS,MinhajuddinAT,IjazA,etal.Associationofurinarysodium/potassiumratiowithbloodpressure:sexandracialdifferences.ClinJAmSocNephrol20127:315.

    6. AburtoNJ,HansonS,GutierrezH,etal.Effectofincreasedpotassiumintakeoncardiovascularriskfactorsanddisease:systematicreviewandmetaanalyses.BMJ2013346:f1378.

    7. WheltonPK,HeJ,CutlerJA,etal.Effectsoforalpotassiumonbloodpressure.Metaanalysisofrandomizedcontrolledclinicaltrials.JAMA1997277:1624.

    8. AvivA,HollenbergNK,WederA.Urinarypotassiumexcretionandsodiumsensitivityinblacks.Hypertension200443:707.

    9. TurbanS,MillerER3rd,AngeB,AppelLJ.Racialdifferencesinurinarypotassiumexcretion.JAmSocNephrol200819:1396.

    10. FrisanchoAR,LeonardWR,BollettinoLA.Bloodpressureinblacksandwhitesanditsrelationshiptodietarysodiumandpotassiumintake.JChronicDis198437:515.

    11. AdroguHJ,MadiasNE.Sodiumandpotassiuminthepathogenesisofhypertension.NEnglJMed2007356:1966.

    12. AppelLJ,GilesTD,BlackHR,etal.ASHpositionpaper:dietaryapproachestolowerbloodpressure.JAmSocHypertens20104:79.

    13. BianchettiMG,WeidmannP,BerettaPiccoliC,FerrierC.Potassiumandnorepinephrineorangiotensinmediatedpressorcontrolinprehypertension.KidneyInt198731:956.

    14. GallenIW,RosaRM,EsparazDY,etal.Onthemechanismoftheeffectsofpotassiumrestrictiononbloodpressureandrenalsodiumretention.AmJKidneyDis199831:19.

    15. HeFJ,MarkanduND,ColtartR,etal.Effectofshorttermsupplementationofpotassiumchlorideandpotassiumcitrateonbloodpressureinhypertensives.Hypertension200545:571.

    16. HeFJ,MarciniakM,CarneyC,etal.Effectsofpotassiumchlorideandpotassiumbicarbonateonendothelialfunction,cardiovascularriskfactors,andboneturnoverinmildhypertensives.Hypertension201055:681.

    Topic3876Version11.0

    potassium/dayprovidedtheydonothaveapredispositiontohyperkalemia.Thislevelofpotassiumintakecanbeachievedpreferablywithdietarycounseling.(See'Clinicalimplications'above.)

  • 19/4/2015 Potassiumandhypertension

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    GRAPHICS

    IontransportinloopofHenle

    SchematicrepresentationofthetransportmechanismsinthethickascendinglimboftheloopofHenle.TheNaKATPasepumpinthebasolateral(peritubular)membranepumpssodium(Na)outof,andpotassium(K)into,thecell.ThiscreatesalowintracellularNaconcentrationwhichdrivesmanyofthecell'sreabsorptiveprocesses.Theentryoffilteredsodiumchloride(NaCl)intothecellsismediatedbyanelectroneutralNaK2Cl(NKCC2)cotransporterintheapical(luminal)membrane.Thisisalsocalledthefurosemidesensitivecotransporter.TheenergyforthisprocessisprovidedbythefavorableinwardelectrochemicalgradientforNa(theintracellularNaconcentrationisverylowandthecellinterioriselectronegative).TheinwardmovementofKandCloccursagainsttheirelectrochemicalgradientsandispoweredbytheinwardmovementofNaintothecell.ThereabsorbedNawhichhasenteredthecellispumpedoutbytheNaKATPasepump.TheconcentrationofKinthefiltrateandtubularfluidismuchlowerthanthatofNaandCl,andmuchofthereabsorbedKrecyclebackintothelumenthroughKchannels(ROMK)intheapicalmembranetoallowcontinuedNaClreabsorption.ThismovementofcationicKintothelumenplusthefluxofreabsorbedCloutofthecellintotheperitubularcapillary(viaClchannels)causesthelumentobecomemorepositivelychargedcomparedwiththecellandperitubularspace.ThislumenelectropositivitycreatesanelectricalgradientthatpromotesthepassivereabsorptionofcationsNa,calcium(Ca),andmagnesium(Mg)viatheparacellularpathwaybetweenthecells.ThemostimportantClchannelsinthesecellsareClCKb.AlsopresentbutnotascriticalaretheClCKachannels.EachoftheseClchannelsrequiresinteractionwithasmallproteincalledbarttintofunctionnormally.ThesingleClchannelshowninthefigurerepresentsbothintactClCKaandClCKbchannels.

    Graphic75301Version9.0

  • 19/4/2015 Potassiumandhypertension

    http://www.uptodate.com/contents/potassiumandhypertension?topicKey=NEPH%2F3876&elapsedTimeMs=0&source=search_result&searchTerm=pota 5/5

    Disclosures:NormanMKaplan,MDNothingtodisclose.DavidBMount,MDConsultant/AdvisoryBoards:ZSPharma[Potassiumbinders(ZS9,preclinical)].hyperkalemia].Consultant/AdvisoryBoards:MedtronicRelypsaBayerNovartisDSIBoehringerIngelheimLexiconJanssenAstraZenecaKona[Diabetes,hyperkalemia,resistanthypertension(Canagliflozin,dapagliflozin,empagliflozin)].Nothingtodisclose.Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseareaddressedbyvettingthroughamultilevelreviewprocess,andthroughrequirementsforreferencestobeprovidedtosupportthecontent.AppropriatelyreferencedcontentisrequiredofallauthorsandmustconformtoUpToDatestandardsofevidence.Conflictofinterestpolicy

    Disclosures


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