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(Hypertension. 2004;44:253.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?

From the Division of Clinical Gene Therapy, Graduate School of Medicine, Osaka University, Japan.

Correspondence to Ryuichi Morishita, MD, PhD, Professor, Division of Clinical Gene Therapy, Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565, Japan. E-mail morishit@cgt.med.osaka-u.ac.jp

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Hypertension substantially increases the risk for coronary heart disease, stroke, retinopathy, and nephropathy. In patients, hypertension usually clusters with the other components of the metabolic syndrome, such as microalbuminuria, central obesity, insulin resistance, dyslipidemia, hypercoagulation, increased inflammation, and left ventricular hypertrophy. Of importance, obesity, atherosclerosis, insulin resistance, hyperinsulinemia, hyperlipidemia, essential hypertension, type 2 diabetes mellitus, and for coronary heart disease are components of the metabolic syndrome and are associated with elevated plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-, which are markers of inflammation. This suggests that the metabolic syndrome is a low-grade, systemic, inflammatory condition. Hence, instituting antiinflammatory measures might be beneficial in preventing or halting the progression of the metabolic syndrome in high-risk populations.

Therefore, numerous studies have been conducted to identify the relationship between hypertension and inflammation. Clinical data demonstrated that hypertension is clearly linked to inflammation, because C-reactive protein levels are reported to be associated with future development of hypertension.^1,2 In addition, basic and clinical research have also demonstrated that upregulation of genes related to inflammation, such as tumor necrosis factor-, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1, to name a few, was observed in target organs and/or circulation of hypertensive animals and patients.^3–6 Increase in tissue and/or circulating levels of inflammatory cytokines suggest that the production of these cytokines increases the risk of plaque rapture.

However, how hypertension causes inflammation is not clear. Does high blood pressure directly cause inflammation, or do other humoral factors related to hypertension promote inflammation? . . . [Full Text of this Article]

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