Abstract

Abstract Hypertension is a risk factor for the development of atherosclerosis, although the mechanisms have not been well elucidated. As the cellular and molecular mechanisms of the pathogenesis of atherosclerosis and the effects of hypertension are being more clearly defined, it becomes apparent that the two processes have certain common mechanisms. The endothelium is a likely central focus for the effect of both diseases. There is increasing evidence that atherosclerosis should be viewed fundamentally as an inflammatory disease. Atherogenic stimuli such as hyperlipidemia appear to activate the inflammatory response by causing expression of mononuclear leukocyte recruiting mechanisms. The gene for one of these, the vascular cell adhesion molecule-1, is controlled at least in part by transcriptional factors regulated by oxidative stress, which modifies the redox state of the endothelial cell. Alterations in the redox state of the arterial wall also may contribute to vascular smooth muscle cell growth. In a somewhat parallel fashion, there is evidence that hypertension may also exert oxidative stress on the arterial wall. This article reviews evidence that leads to the postulate that hypertension predisposes to and accelerates atherosclerosis at least in part because of synergy between elevated blood pressure and other atherogenic stimuli to induce oxidative stress on the arterial wall.

Keywords

PathogenesisOxidative stressHyperlipidemiaEndotheliumMedicineInflammationArterial wallCell adhesion moleculeVascular wallInternal medicineImmunologyEndocrinology

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Publication Info

Year
1995
Type
review
Volume
25
Issue
2
Pages
155-161
Citations
772
Access
Closed

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R. Wayne Alexander (1995). Hypertension and the Pathogenesis of Atherosclerosis. Hypertension , 25 (2) , 155-161. https://doi.org/10.1161/01.hyp.25.2.155

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DOI
10.1161/01.hyp.25.2.155