Journal
HYPERTENSION
Volume 35, Issue 1, Pages 86-90Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.HYP.35.1.86
Keywords
endothelium-derived factor; growth substances; inflammation; adhesion molecule; angiotensin II; fibrosis
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We previously reported that chronic inhibition of nitric oxide (NO) synthesis with N-omega-nitro-L-arginine methyl ester (L-NAME) induces inflammatory changes (monocyte infiltration, myofibroblast formation, and monocyte chemoattractant protein-1 [MCP-1] and transforming growth factor-beta 1 [TGF-beta 1] expression) in the rat heart and vessel. There is debate regarding whether TGF-beta 1 exhibits proinflammatory or anti-inflammatory activities. We used the rat model to investigate the role of TGF-beta in the pathogenesis of such inflammatory changes. We show here that infiltrating monocytes and myofibroblasts in the inflammatory lesions produced TGF-beta 1 on the third day of L-NAME administration. Cotreatment with a monoclonal antibody against TGF-beta 1, but not with control IgG, prevented the L-NAME-induced cardiac inflammation. The antibody also significantly inhibited the gene expression of MCP-1, P-selectin, and intercellular adhesion molecule-1. In summary, the antibody against TGF-beta 1 prevented inflammatory changes in rat heart and vessel induced by chronic inhibition of NO synthesis, suggesting that increased production of TGF-beta 1 is involved in the: inflammatory changes in this model.
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