Figure 6.

The proposed mechanism of renal Ang II generation and its function. (A) In normal conditions, a portion of plasma Agt is filtered through glomeruli and reabsorbed by proximal convoluted tubules (PCT) via megalin. However, the reabsorbed Agt is not converted to Ang II. Agt is synthesized in proximal straight tubules (PST), but this Agt makes little contribution to renal Ang II. Renal Ang II is probably generated from liver-derived Agt in the capillary lumen or interstitium. (B) In nephrotic syndrome, podocyte injury increases glomerular leakage of plasma Agt. The filtered Agt is absorbed by proximal tubules via megalin and thereafter converted to Ang II. The increased renal Ang II may contribute to sodium retention possibly by activating NHE3 and ENaC, although direct action on these molecules has not been proven.