The renin-angiotensin-aldosterone system (RAAS) plays a critical role in kidney function and its inhibition reduces proteinuria and preserves kidney function in patients with chronic kidney disease. Recent studies have shown that podocytes generate many components of the RAAS and they express receptors of RAAS, including angiotensin II, mineralocorticoid, and prorenin receptors. Crucial functions of podocytes, such as contraction, apoptosis, autophagocytosis, and cytoskeletal organization, have been shown to be regulated by the angiotensin II type 1 receptors. An activation of the glomerular RAAS and protection from podocyte injury by RAAS inhibitors have been shown in many glomerular diseases. Exploring the interaction between the local RAAS and the signaling involved in RAAS activation in podocytes will lead to new therapeutic strategies of podocyte protection.