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SystemicHypertensioncont.
Page1:ArterialPressure
Page2:HypertensionCategories
THISPAGE:CausesofHypertension
Page4:AntihypertensiveDrugs

CausesofHypertension

Thearetwobasictypesofhypertension:primary(essential)hypertensionandsecondaryhypertension.Thevast
majorityofpatients(9095%)haveessentialhypertension,whichisaformwithnoidentifiableunderlying
cause.Thisformofhypertensioniscommonlytreatedwithdrugsinadditiontolifestylechanges(e.g.,exercise,
propernutrition,weightreduction,stressreduction).

Asmallernumberofpatients(510%)havesecondaryhypertensionthatiscausedbyanidentifiableunderlying
conditionsuchasrenalarterydisease,thyroiddisease,primaryhyperaldosteronism,pregnancy,etc.

Somecausesofsecondaryhypertensionarelistedbelow:

Renalarterystenosis
Chronicrenaldisease
Primaryhyperaldosteronism
Stress
Sleepapnea
Hyperorhypothyroidism
Pheochromocytoma
Preeclampsia
Aorticcoarctation

Renalarterystenosis(renovasculardisease)

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Renalarterydiseasecancauseofnarrowingofthevessellumen(stenosis).Thereducedlumendiameter
increasesthepressuredropalongthelengthofthediseasedartery,whichreducesthepressureattheafferent
arterioleinthekidney.Reducedarteriolarpressureandreducedrenalperfusionstimulatereninreleasebythe
kidney.ThisincreasescirculatingangiotensinII(AII)andaldosterone.Thesehormonesincreasebloodvolume
byenhancingrenalreabsorptionofsodiumandwater.IncreasedAIIcausessystemicvasoconstrictionand
enhancessympatheticactivity.ChronicelevationofAIIpromotescardiacandvascularhypertrophy.Thenet
effectoftheserenalmechanismsisanincreaseinbloodvolumethataugmentscardiacoutputbytheFrank
Starlingmechanism.Therefore,hypertensioncausedbyrenalarterystenosisresultsfrombothanincreasein
systemicvascularresistanceandanincreaseincardiacoutput.

Chronicrenaldisease
Anynumberofpathologicprocesses(e.g.,diabeticnephropathy,glomerulonephritis)candamagenephronsin
thekidney.Whenthisoccurs,thekidneycannotexcretenormalamountsofsodiumwhichleadstosodiumand
waterretention,increasedbloodvolume,andincreasedcardiacoutputbytheFrankStarlingmechanism.Renal
diseasemayalsoresultinincreasedreleaseofreninleadingtoarenindependentformofhypertension.The
elevationinarterialpressuresecondarytorenaldiseasecanbeviewedasanattemptbythekidneytoincrease
renalperfusionandrestoreglomerularfiltration.

Primaryhyperaldosteronism

Increasedsecretionofaldosteronegenerallyresultsfromadrenaladenomaoradrenalhyperplasia.Increased
circulatingaldosteronecausesrenalretentionofsodiumandwater,sobloodvolumeandarterialpressure
increase.Plasmareninlevelsaregenerallydecreasedasthebodyattemptstosuppressthereninangiotensin
systemthereisalsohypokalemiaassociatedwiththehighlevelsofaldosterone.

Stress
Emotionalstressleadstoactivationofthesympatheticnervoussystem,whichcausesincreasedreleaseof
norepinephrinefromsympatheticnervesintheheartandbloodvessels,leadingtoincreasedcardiacoutputand
increasedsystemicvascularresistance.Furthermore,theadrenalmedullasecretesmorecatecholamines
(epinephrineandnorepinephrine).Activationofthesympatheticnervoussystemincreasescirculating
angiotensinII,aldosterone,andvasopressin,whichcanincreasesystemicvascularresistance.Prolonged
elevationofangiotensinIIandcatecholaminescanleadtocardiacandvascularhypertrophy,bothofwhichcan
contributetoasustainedincreaseinbloodpressure.

SleepApnea

Sleepapneaisadisorderinwhichpeoplerepeatedlystopbreathingforshortperiodsoftime(1030seconds)
duringtheirsleep.Thisconditionisoftenassociatedwithobesity,althoughitcanhaveothercausessuchas
airwayobstructionordisordersofthecentralnervoussystem.Theseindividualshaveahigherincidenceof
hypertension.Themechanismofhypertensionmayberelatedtosympatheticactivationandhormonalchanges

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associatedwithrepeatedperiodsofapneainducedhypoxiaandhypercapnea,andfromstressassociatedwith
thelossofsleep.

Hyperorhypothyroidism
Excessivethyroidhormoneinducessystemicvasoconstriction,anincreaseinbloodvolume,andincreased
cardiacactivity,allofwhichcanleadtohypertension.Itislessclearwhysomepatientswithhypothyroidism
develophypertension,butitmayberelatedtodecreasedtissuemetabolismreducingthereleaseofvasodilator
metabolites,therebyproducingvasoconstrictionandincreasedsystemicvascularresistance.

Pheochromocytoma

Catecholaminesecretingtumorsintheadrenalmedullacanleadtoveryhighlevelsofcirculating
catecholamines(bothepinephrineandnorepinephrine).Thisleadstoalphaadrenoceptormediatedsystemic
vasoconstrictionandbetaadrenoceptormediatedcardiacstimulation,bothofwhichcontributetosignificant
elevationsinarterialpressure.Despitetheelevationinarterialpressure,tachycardiaoccursbecauseofthe
directeffectsofthecatecholaminesontheheartandvasculature.Excessivebetaadrenoceptorstimulationin
theheartoftenleadstoarrhythmias.Thepheochromocytomaisdiagnosedbymeasuringplasmaorurine
catecholaminelevelsandtheirmetabolites(vanillylmandelicacidandmetanephrine).

Preeclampsia
Thisisaconditionthatsometimesdevelopsduringthethirdtrimesterofpregnancythatcauseshypertensiondue
toincreasedbloodvolumeandtachycardia.TheformerincreasescardiacoutputbytheFrankStarling
mechanism.

Aorticcoarctation

Coarctation,ornarrowingoftheaorta(typicallyjustdistaltotheleftsubclavianartery),isacongenitaldefect
thatobstructsaorticoutflowleadingtoelevatedpressuresproximaltothecoarctation(i.e.,elevatedarterial
pressuresintheheadandarms).Distalpressures,however,arenotnecessarilyreducedaswouldbeexpected
fromthehemodynamicsassociatedwithastenosis.Thereasonforthisisthatreducedsystemicbloodflow,and
inparticularreducedrenalbloodflow,leadstoanincreaseinthereleaseofreninandanactivationoftherenin
angiotensinaldosteronesystem.Thisinturnelevatesbloodvolumeandarterialpressure.Althoughtheaortic
archandcarotidsinusbaroreceptorsareexposedtohigherthannormalpressures,thebaroreceptorreflexis
bluntedduetostructuralchangesinthewallsofvesselswherethebaroreceptorsarelocated.Also,
baroreceptorsbecomedesensitizedtochronicelevationinpressureandbecome"reset"tothehigherpressure.

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AntihypertensiveDrugs

Revised06/17/08

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