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From molecular plasticity of vascular cells to tissue remodeling: example of the L-NAME model |
Sang Thrombose Vaisseaux. Volume 11, Number 9, 653-9, Novembre 1999, Mini-revues
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 Résumé
Article gratuit
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Author(s) : Jean-Baptiste Michel |
Summary : The chronic blockade of nitric oxide production by L-NAME induces important modifications of vasomotor tone and a pro-inflammatory remodeling of the arterial wall leading to a short life expectancy of the animals. Premature deaths are related to ischemic accidents in different target tissues: stroke in the central nervous system, fibrosis in the heart and kidney. In the heart and the kidney the pathological phenomenon leads to a progressive loss of function. The chronic blockade of NO production and associated hypertension lead to the development of a perivascular inflammatory infiltration. They are also associated with an increase in monocyte adhesion at the luminal pole of the arteries. Perivascular inflammation is probably involved in the development of perivascular fibrosis via the production of TGF-beta. This inflammation is due to the appearance of a pro-inflammatory phenotype within the arterial wall, related to the expression of genes, not usually expressed in the vascular wall under physiological conditions, but induced by the absence of NO and the presence of hypertension. Among these are inducible type II NO synthase, the type II isoform of cyclo oxygenase, inducible adhesion molecules (VCAM), Monocyte Chemotactic Protein (MCP-1)… The induction of these genes appears to be secondary to the activation of the NF-kappa-B system in the smooth muscle cells, related to the chronic change in the redox status of the target vascular cells. These mechanisms are similar to those observed in atherosclerosis and could provide the link between hypertension, endothelial dysfunction and atherosclerotic risk. |
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