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Beyond blood pressure: the endothelium and atherosclerosis progression.
Am J Hypertens 2002; 15(10 Pt 2):115S-122SAJ

Abstract

Endothelial dysfunction and remodeling of the vessel wall of large and small arteries is associated with hypertension and other risk factors for cardiovascular disease. These changes alter vascular function and mechanics, aggravate high blood pressure (BP), and may accelerate the progression of atherosclerosis. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide (NADH) oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessels to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation. Upregulation of endothelin-1, adhesion molecules, nuclear factor-kappaB, and other inflammatory mediators, as well as increased breakdown of nitric oxide and uncoupling of nitric oxide synthase, contribute to the progression of vascular disease and atherogenesis. Clinical studies in which treatment with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) was used demonstrated correction of some of the changes in large and small arteries in hypertensive subjects, whereas identical BP lowering with beta-blockers had no effect on endothelial function. In experimental models of atherosclerosis, ARBs, including losartan potassium, valsartan, and olmesartan medoxomil, have demonstrated the ability to prevent the progression of atherosclerosis. This was in part associated with decreased expression of inflammatory mediators and improved endothelial function. Blockade of the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs appears to blunt both the development and progression of vascular disease in both small and large vessels in experimental models and in humans beyond the effect of these agents on BP. This may help to explain the positive results of recently completed trials such as Heart Outcomes Prevention Evaluation (HOPE) and Losartan Intervention for Endpoint Reduction in Hypertension (LIFE).

Authors+Show Affiliations

Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada. schiffe@ircm.qc.caNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

12383592

Citation

Schiffrin, Ernesto L., and Canadian Institutes of Health Research Multidisciplinary Research Group on Hypertension. "Beyond Blood Pressure: the Endothelium and Atherosclerosis Progression." American Journal of Hypertension, vol. 15, no. 10 Pt 2, 2002, 115S-122S.
Schiffrin EL, Canadian Institutes of Health Research Multidisciplinary Research Group on Hypertension. Beyond blood pressure: the endothelium and atherosclerosis progression. Am J Hypertens. 2002;15(10 Pt 2):115S-122S.
Schiffrin, E. L. (2002). Beyond blood pressure: the endothelium and atherosclerosis progression. American Journal of Hypertension, 15(10 Pt 2), 115S-122S.
Schiffrin EL, Canadian Institutes of Health Research Multidisciplinary Research Group on Hypertension. Beyond Blood Pressure: the Endothelium and Atherosclerosis Progression. Am J Hypertens. 2002;15(10 Pt 2):115S-122S. PubMed PMID: 12383592.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beyond blood pressure: the endothelium and atherosclerosis progression. AU - Schiffrin,Ernesto L, AU - ,, PY - 2002/10/18/pubmed PY - 2003/3/4/medline PY - 2002/10/18/entrez SP - 115S EP - 122S JF - American journal of hypertension JO - Am. J. Hypertens. VL - 15 IS - 10 Pt 2 N2 - Endothelial dysfunction and remodeling of the vessel wall of large and small arteries is associated with hypertension and other risk factors for cardiovascular disease. These changes alter vascular function and mechanics, aggravate high blood pressure (BP), and may accelerate the progression of atherosclerosis. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate (NADPH)/nicotinamide adenine dinucleotide (NADH) oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessels to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation. Upregulation of endothelin-1, adhesion molecules, nuclear factor-kappaB, and other inflammatory mediators, as well as increased breakdown of nitric oxide and uncoupling of nitric oxide synthase, contribute to the progression of vascular disease and atherogenesis. Clinical studies in which treatment with angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) was used demonstrated correction of some of the changes in large and small arteries in hypertensive subjects, whereas identical BP lowering with beta-blockers had no effect on endothelial function. In experimental models of atherosclerosis, ARBs, including losartan potassium, valsartan, and olmesartan medoxomil, have demonstrated the ability to prevent the progression of atherosclerosis. This was in part associated with decreased expression of inflammatory mediators and improved endothelial function. Blockade of the renin-angiotensin-aldosterone system with ACE inhibitors or ARBs appears to blunt both the development and progression of vascular disease in both small and large vessels in experimental models and in humans beyond the effect of these agents on BP. This may help to explain the positive results of recently completed trials such as Heart Outcomes Prevention Evaluation (HOPE) and Losartan Intervention for Endpoint Reduction in Hypertension (LIFE). SN - 0895-7061 UR - https://www.unboundmedicine.com/medline/citation/12383592/Beyond_blood_pressure:_the_endothelium_and_atherosclerosis_progression_ L2 - https://academic.oup.com/ajh/article-lookup/doi/10.1016/s0895-7061(02)03006-6 DB - PRIME DP - Unbound Medicine ER -