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Vascular inflammation: a role in vascular disease in hypertension?
Curr Opin Nephrol Hypertens 2003; 12(2):181-7CO

Abstract

PURPOSE OF REVIEW

In this review, we summarize the more recent clinical evidence highlighting the importance of vascular inflammation in terms of clinical risk prediction, and the mechanisms mediating the upregulation of inflammatory mediators in cardiovascular disease and hypertension.

RECENT FINDINGS

Markers of inflammation have been shown to be upregulated in different forms of cardiovascular disease, and to correlate with vascular risk. Atherosclerosis is characterized by chronic inflammation of the vascular wall. The I-kappaB/nuclear factor-kappaB system is considered a major intracellular inflammatory pathway, mediating most of the vascular inflammatory responses. Increasing evidence indicates that hypertension, through the vasoactive peptides angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies proinflammatory properties of angiotensin II have been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. The angiotensin II receptors involved in the inflammatory process and the interaction between angiotensin II and nitric oxide in mediating vascular inflammation have been identified. In addition, recent advances concerning the role of endothelin-1 as another important mediator of chronic inflammation in the vascular wall has been documented, and the relationship between endothelin-1 and angiotensin II on vascular inflammation demonstrated.

SUMMARY

Inflammatory mechanisms are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of useful markers of inflammation, of new therapeutic targets to interfere with these mechanisms, and the evaluation of the efficacy of antiinflammatory treatments will allow progress in our ability to combat cardiovascular disease and the complications of hypertension.

Authors+Show Affiliations

Multidisciplinary Research Group on Hypertension, Quebec, Canada.No affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

12589179

Citation

Virdis, Agostino, and Ernesto L. Schiffrin. "Vascular Inflammation: a Role in Vascular Disease in Hypertension?" Current Opinion in Nephrology and Hypertension, vol. 12, no. 2, 2003, pp. 181-7.
Virdis A, Schiffrin EL. Vascular inflammation: a role in vascular disease in hypertension? Curr Opin Nephrol Hypertens. 2003;12(2):181-7.
Virdis, A., & Schiffrin, E. L. (2003). Vascular inflammation: a role in vascular disease in hypertension? Current Opinion in Nephrology and Hypertension, 12(2), pp. 181-7.
Virdis A, Schiffrin EL. Vascular Inflammation: a Role in Vascular Disease in Hypertension. Curr Opin Nephrol Hypertens. 2003;12(2):181-7. PubMed PMID: 12589179.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vascular inflammation: a role in vascular disease in hypertension? AU - Virdis,Agostino, AU - Schiffrin,Ernesto L, PY - 2003/2/18/pubmed PY - 2004/10/20/medline PY - 2003/2/18/entrez SP - 181 EP - 7 JF - Current opinion in nephrology and hypertension JO - Curr. Opin. Nephrol. Hypertens. VL - 12 IS - 2 N2 - PURPOSE OF REVIEW: In this review, we summarize the more recent clinical evidence highlighting the importance of vascular inflammation in terms of clinical risk prediction, and the mechanisms mediating the upregulation of inflammatory mediators in cardiovascular disease and hypertension. RECENT FINDINGS: Markers of inflammation have been shown to be upregulated in different forms of cardiovascular disease, and to correlate with vascular risk. Atherosclerosis is characterized by chronic inflammation of the vascular wall. The I-kappaB/nuclear factor-kappaB system is considered a major intracellular inflammatory pathway, mediating most of the vascular inflammatory responses. Increasing evidence indicates that hypertension, through the vasoactive peptides angiotensin and endothelin-1, promotes and accelerates the atherosclerotic process via inflammatory mechanisms. In animal and human studies proinflammatory properties of angiotensin II have been demonstrated in large conduit and small arteries, in the kidney as well as in the heart. The angiotensin II receptors involved in the inflammatory process and the interaction between angiotensin II and nitric oxide in mediating vascular inflammation have been identified. In addition, recent advances concerning the role of endothelin-1 as another important mediator of chronic inflammation in the vascular wall has been documented, and the relationship between endothelin-1 and angiotensin II on vascular inflammation demonstrated. SUMMARY: Inflammatory mechanisms are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of useful markers of inflammation, of new therapeutic targets to interfere with these mechanisms, and the evaluation of the efficacy of antiinflammatory treatments will allow progress in our ability to combat cardiovascular disease and the complications of hypertension. SN - 1062-4821 UR - https://www.unboundmedicine.com/medline/citation/12589179/Vascular_inflammation:_a_role_in_vascular_disease_in_hypertension L2 - http://dx.doi.org/10.1097/00041552-200303000-00009 DB - PRIME DP - Unbound Medicine ER -