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CARDOSO, V. G. A Angiotensina II promove o aumento da atividade do NHE1 pela via de sinalização intracelular da p38 mapk e promove apoptose por alcalinização do citosol em podócitos. 2016. 60 p. Masters thesis (Human Physiology) Instituto de Ciências Biomédicas, Universidade de São Paulo, 2016. It has been observed that high plasma, or kidney tissue concentrations of angiotensin II (Ang II) leads to changes in renal hemodynamics, severe glomerular injury, increased synthesis of glomerular extracellular matrix components, oxidative stress and apoptosis in glomerular cells, including podocyte and mesangial cells. Podocytes a local renin-angiotensin system (RAS), expresses the AT1 and AT2 receptors for Ang II and the Na + / H + exchanger (NHE1). The NHE1 is involved with resistance and induction of apoptosis, cell volume control and maintenance of cell phenotype. Thus, the goal of this study was to investigate in podocytes the role of Ang II in the induction of apoptosis, and intracellular events linked to the NHE1 activity in this condition. Our results indicate that the treatment with Ang II, in a high dose, for 24 hours induces apoptosis in podocytes, and promotes oxidative stress. However, the activation of NADPH oxidase subunits Nox4 and p22 (phox) and proapoptotic pprotein Bax, came before the late apoptosis observed in 24 hours of treatment with Ang II. Under physiological conditions, the NHE1 activity contributes to cell survival by preventing cytosolic acidification. Moreover, Ang II via the AT1 receptor, activates intracellular signaling pathway p38 MAPK and increases the NHE1 activiy leading to alkalosis, Bax activation and apoptosis in podocytes.

A angiotensina II promove o aumento da atividade do NHE1 pela via de sinalização intracelular da P38 MAPK e promove apoptose por alcalinização do citosol em podócitos.