I will revise the established links between, aging, telomerase deficiency, redox imbalance, hypertension and renal dysfunction. Telomere shortening increases with aging, and telomere length is lower in aging hypertensive than in aging normotensive individuals. Mice lacking the mTerc telomerase component (Terc^-/-) are a useful model to study mechanisms of aging. Terc^-/-mice show hypertension and signs of renal aging such as reduced renal function and renal fibrosis. Kidney tissue and mouse embryonic fibroblast (MEF) from these animals show increased H₂O₂ production and decreased catalase activity and mRNA expression. Restoration of the telomerase activity in MEF by transfection with mTerc telomerase restores the catalase expression and activity and diminishes H₂O₂ production, indicating a direct link between telomerase and catalase deficiencies. Terc^-/- mice also showed hypertension caused by increased circulating levels of endothelin-1 (ET-1), that was based in an increased ET-1 converting enzyme (ECE-1) expression without changes in ET-1. MEF from Terc^-/- mice shows decreased catalase expression, increased H₂O₂ content and increased ECE-1 expression, that was corrected by incubation with catalase or antioxidants.

These results suggest that mice lacking telomerase activity show hypertension and renal damage due to an increase of plasma ET-1 levels, as a consequence of ECE-1 overexpression, which is based in a reduced catalase activity and increased H₂O₂ content. Mice KO for catalase shows also renal damage. Thus, it is possible to deduce a direct link between aging, telomerase activity, increased oxidative stress, renal damage and hypertension.