Vascular inflammation: a role in vascular disease in hypertension?
OBJECTIVE
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.


RESULTS
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.


CONCLUSIONS
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.
Virdis
Agostino
A
Multidisciplinary Research Group on Hypertension, Quebec, Canada.
Schiffrin
Ernesto L
EL
D000804:Angiotensin II / Q000378:metabolism / Q000502:physiology*; D001161:Arteriosclerosis / Q000209:etiology* / Q000503:physiopathology; D016232:Endothelins / Q000378:metabolism / Q000502:physiology; D004730:Endothelium, Vascular / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D011237:Predictive Value of Tests; D011379:Prognosis; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D014652:Vascular Diseases / Q000150:complications / Q000175:diagnosis; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism* / Q000502:physiology
D016232:Endothelins; D018836:Inflammation Mediators; D042461:Vascular Endothelial Growth Factor A; D000804:Angiotensin II; D009569:Nitric Oxide