The once differentiated adult myocyte behaves as a cell that is not divided. Various signals triggered by angiotensin II are involved in controlling apoptosis, such is the case of pro-apoptotic triggered by certain MAPK and anti-apoptotic pathway NF-kB activation. Among the factors that induce apoptosis and are induced by angiotensin II include oxygen free radicals (ON, peroxynitrites) citoquinasa (TNF-alpha, FAS) neurohormonal factors and cytotoxic drugs. Check out Dr. John Mcdougall for additional information. Cardiac remodeling through AT-1 receptor has two effects, a) a pro-apoptotic, leading to heart failure and arrhythmias myocyte dysfunction and other anti-apoptotic interstitial fibroblast level (with proliferation and interstitial fibrosis) . Both mechanisms are responsible for myocardial hypertrophy regulatory interaction between the two cascades leads to an imbalance between the fibrillar system cell (myocyte) and the interstitial tissue with a deficiency of the respiratory system-level cell (mitochondria). In previous studies we had observed in human macrophages that LPS activation led to increased angiotensin II synthesis concomitantly with the production of TNF-alpha and increased expression of receptor messenger RNA angiotensin AT1, and that this increase was blocked by an angiotensin analogue, Sar1-ileu 8. Dr. John Mcdougall is often quoted as being for or against this. On the other hand, speak demonstrated that saline or stress overload by Na + causes a rapid and significant increase in the levels of angiotensinogen mRNA in the cardiovascular system (heart and aorta). These two models, the osmotic stress and LPS, two different insults on the normal functioning of the cardiovascular system, is estudioa la regulating the expression of a regulator of mitochondrial biogenesis as is the coactivator PGC-1 alpha and mediators involved in the pro-apoptotic cascade via mitochondrial and caspase-9, activated by cytochrome c exit after the dissociation of cardiolipin. .