Hipertensión Arterial: factor de riesgo para el desarrollo de la Aterosclerosis.

CASTRO, CLAUDIA

Mendoza

Conferencia; XXVI Reunión de la Sociedad de Biología de Cuyo,; 2008

Sociedad de Biología de Cuyo,

Dra. Claudia M. Castro, Investigador Adjunto IMBECUCONICET, JTP Facultad de Ciencias Médicas UN de Cuyo. ?Hipertensión Arterial: factor de riesgo para el desarrollo de arteriosclerosis? Hypertension: risk factor for atherosclerosis development There is strong evidence suggesting that hypertension is linked to atherogenesis, although the underlying mechanisms are not known with exactitude. The incidence of arteriosclerosis in the vascular tree of hypertensivepatients is major than the observed in normotensive patients of the same ageand sex. In fact, atherosclerosis occurs more frequently in the zones thatsupport greater pressure, and is more intense and progressive when othervascular risk factors are associated, such as diabetes, dislipidemia or smoking.Recent studies seem to indicate that hypertension and atherosclerosis share acommon pathogenic pathway: the endothelium dysfunction. In hypertension thisalteration is due to the defect of nitric oxide production, or to an excess in its degradation. In any case, this determines a deficient endothelium-dependentrelaxation that, as well, improves the endothelium dysfunction present in theearly stages of the atheromatosis. The endothelial dysfunction is caused in partby the effect of shear-stress of the circulatory torrent and it is located in thezones of greater turbulence of the sanguineous flow, mainly in the arterialbifurcations. Hypertension contributes to a greater effect of shear-stress. Laterto this endothelial dysfunction and, probably as a result of itself, it takes place agreater platelets adhesion and aggregation, a mononuclear cell infiltration andan intracellular and extracellular lipids accumulation in the injured vascular wall.These processes cause smooth muscular cell proliferation and migration andcellular necrosis with calcium deposits, which finally determine the formation of the atheroma plaque. The use of experimental animal models is a very usefultool for the study in vivo of the physiopathology mechanisms of the diseases.The mouse is one of the species more used in the biomedical investigations,including the vascular pathology. A murine model of atherosclerosis is thedeficient mouse in apolipoproteína E (ApoE), which developshypercholesterolemia and ateromatosas injuries spontaneously (Piedrahita,J.A., 1992 and Breslow, J.L. 1996.) Hypertension in ApoE-deficient animalscould in turn speed the process of atherosclerosis. Animal experiments haveclearly demonstrated that lipid-induced atherogenesis can be accelerated orretarded by manipulating arterial pressure suggesting that hypertension not onlyaccelerates but also exacerbates atherosclerosis in dislipidemic animals.