Figure 7
From: Angiotensin II increases glomerular permeability by β-arrestin mediated nephrin endocytosis
This scheme of function depicts how Ang II promotes glomerular permeability by nephrin endocytosis.
Ang II activates the AT1-receptor (AT1-R). The activated AT1-receptor transfers the signal through Gαq/11 and PLC. In turn nephrin gets phosphorylated at T1120/T1125 forming a β-arrestin2 binding site16. The binding of β-arrestin2 leads to increased nephrin endocytosis. This could be the mode of action how the glomerular permeability is increased beyond hemodynamic effects. In contrast, inhibition of the AT1-receptor by sartans promotes less β-arrestin2 nephrin interaction and less nephrin endocytosis leading to decreased glomerular permeability.
