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Inflammation may be a bridge connecting hypertension and atherosclerosis.
Med Hypotheses 2005; 64(5):925-9MH

Abstract

Pathogenesis of the atherosclerotic process is deemed as multi-factorial, and characterized by chronic inflammatory response. Although hypertension is known to be one of the most important risk factors for atherosclerosis in causasians, its relative contribution to early atherosclerosis are still unknown. Increased evidence has indicated that hypertension, through the vasoactive peptides, such as angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies pro-inflammatory properties of angiotensin II has been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate/nicotinamide adenine dinucleotide oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessel to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation, upregulation of endothelin-1, adhesion molecules, nuclear factor-kappa B, 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. In addition, recent advances concerning role of endothelin-1 as another important mediator of chronic inflammation in the vascular wall has been documented, and relationship between endothelin-1 and angiotensin II on vascular inflammation demonstrated. Inflammatory mechanisms, therefore, are important participants in the pathophysiology of hypertension-related cardiovascular disease, including atherosclerosis. In experimental models as well as human studies of atherosclerosis, angiotensin converting enzyme inhibitors or angiotensin II receptor blockers have demonstrated the ability to prevent or reverse the progression of atherosclerosis, which was in part associated with decreased expression of inflammatory mediators and improve endothelial functions. Based on those increasing evidence, we hypothesize that inflammation may be a bridge connecting hypertension and atherosclerosis.

Authors+Show Affiliations

Department of Cardiology, Fuwai Hospital, Chinese Academy of Medical Science and Cardiovascular Institute, Peking Union Medical College, Beijing 100037, PR China. lijnjn@yahoo.com.cnNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15780486

Citation

Li, Jian-Jun, and Ji-Lin Chen. "Inflammation May Be a Bridge Connecting Hypertension and Atherosclerosis." Medical Hypotheses, vol. 64, no. 5, 2005, pp. 925-9.
Li JJ, Chen JL. Inflammation may be a bridge connecting hypertension and atherosclerosis. Med Hypotheses. 2005;64(5):925-9.
Li, J. J., & Chen, J. L. (2005). Inflammation may be a bridge connecting hypertension and atherosclerosis. Medical Hypotheses, 64(5), pp. 925-9.
Li JJ, Chen JL. Inflammation May Be a Bridge Connecting Hypertension and Atherosclerosis. Med Hypotheses. 2005;64(5):925-9. PubMed PMID: 15780486.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inflammation may be a bridge connecting hypertension and atherosclerosis. AU - Li,Jian-Jun, AU - Chen,Ji-Lin, PY - 2004/09/20/received PY - 2004/10/06/accepted PY - 2005/3/23/pubmed PY - 2005/7/29/medline PY - 2005/3/23/entrez SP - 925 EP - 9 JF - Medical hypotheses JO - Med. Hypotheses VL - 64 IS - 5 N2 - Pathogenesis of the atherosclerotic process is deemed as multi-factorial, and characterized by chronic inflammatory response. Although hypertension is known to be one of the most important risk factors for atherosclerosis in causasians, its relative contribution to early atherosclerosis are still unknown. Increased evidence has indicated that hypertension, through the vasoactive peptides, such as angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies pro-inflammatory properties of angiotensin II has been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. Activation of oxidative stress by angiotensin II is a key component of this process. Angiotensin II stimulates nicotinamide adenine dinucleotide phosphate/nicotinamide adenine dinucleotide oxidase in endothelium, smooth muscle cells, and the adventitia of blood vessel to generate reactive oxygen species, leading to endothelial dysfunction, growth, and inflammation, upregulation of endothelin-1, adhesion molecules, nuclear factor-kappa B, 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. In addition, recent advances concerning role of endothelin-1 as another important mediator of chronic inflammation in the vascular wall has been documented, and relationship between endothelin-1 and angiotensin II on vascular inflammation demonstrated. Inflammatory mechanisms, therefore, are important participants in the pathophysiology of hypertension-related cardiovascular disease, including atherosclerosis. In experimental models as well as human studies of atherosclerosis, angiotensin converting enzyme inhibitors or angiotensin II receptor blockers have demonstrated the ability to prevent or reverse the progression of atherosclerosis, which was in part associated with decreased expression of inflammatory mediators and improve endothelial functions. Based on those increasing evidence, we hypothesize that inflammation may be a bridge connecting hypertension and atherosclerosis. SN - 0306-9877 UR - https://www.unboundmedicine.com/medline/citation/15780486/Inflammation_may_be_a_bridge_connecting_hypertension_and_atherosclerosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-9877(04)00598-5 DB - PRIME DP - Unbound Medicine ER -