Fig.10.5 •Hyaline arteriolosclerosis isassociatedwithbenignhypertension.Itismarkedbyhomogeneous,pinkhyalinethickeningofthearteriolarwalls,withlossofunderlyingstructuraldetail,andluminalnarrowing(see
Fig.10.5A ).ThelesionsstemfromleakageofplasmacomponentsacrossinjuredECsintovesselwalls,andincreasedECMproductionbySMCsinresponsetochronichemodynamicstress.Inthekidneys,thearteriolarnarrowingcausedbyhyalinearteriosclerosisleadstodiffusevascularcompromiseandnephrosclerosis (glomerularscarring).Althoughthevesselsofolderadultpatients(normotensiveorhypertensive)showthesamechanges,hyalinearteriolosclerosisismoregeneralizedandsevereinpatientswithhypertension.Thesamelesionsalsoarecommonindiabeticmicroangiopathy;inthisdisorder,theunderlyingetiologyishyperglycemia-associatedECdysfunction.
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Fig. 10.5 Hypertensivevasculardisease.(A)Hyalinearteriolosclerosis.Thearteriolarwallisthickenedwiththedepositionofamorphousproteinaceousmaterial(hyalinized),andthelumenismarkedlynarrowed.(B)Hyperplasticarteriolosclerosis(“onion-skinning”)(arrow) causingluminalobliteration(periodicacid–Schiffstain).(B, Courtesy of Helmut Rennke, MD, Brigham and Women’s Hospital, Boston, Massachusetts.) •Hyperplastic arteriolosclerosis ismoretypicalofseverehypertension.Vesselsexhibit“onionskin,”concentric,laminatedthickeningofarteriolarwallsandluminalnarrowing(see
Fig.10.5B ).ThelaminationsconsistofSMCsandthickened,reduplicatedbasementmembrane.Inmalignanthypertension,thesechangesareaccompaniedbyfibrinoiddepositsandvesselwallnecrosis(necrotizing arteriolitis), whichareparticularlyprominentinthekidney.
Hypertensionisacommondisorderaffecting25%ofthepopulation;itisamajorriskfactorforatherosclerosis,congestiveheartfailure,andrenalfailure.
Hypertensionmaybeprimary(idiopathic)orlesscommonlysecondarytoanidentifiableunderlyingcondition.Incloseto95%ofcaseshypertensionisidiopathicor“essential.”Theremainingcases(secondaryhypertension)areduetoprimaryrenaldisease,renalarterynarrowing(renovascularhypertension),oradrenaldisorders.
Essentialhypertensionrepresents95%ofcasesandisacomplex,multifactorialdisorder,involvingbothenvironmentalinfluencesandgeneticpolymorphismsthatmayinfluencesodiumresorption,aldosteronepathways,theadrenergicnervoussystem,andtherenin-angiotensinsystem.
Hypertensionoccasionallyiscausedbysingle-genedisordersorissecondarytodiseasesoftherenalarteries,kidneys,adrenalglands,orotherendocrineorgans.
Injury to the vessel wall—and in particular to ECs—is the fundamental basis for the vast majority of vascular disorders. Such injurious stimuli may be biochemical, immunologic, or hemodynamic. The integrated function of ECs—and the underlying SMCs—is critical for the vasculature to respond to various stimuli; such responses can be adaptive or may lead to pathologic lesions. Thus, EC injury or dysfunction (as discussed earlier) contributes to a host of pathologic processes including thrombosis, atherosclerosis, and hypertensive vascular lesions. Ensuing SMC proliferation and matrix synthesis can help to repair a damaged vessel wall, but also can eventually lead to luminal occlusion.