Although mechanisms of DOCS-induced damage to target organs (heart, kidney, vessels, etc.)remain largely unsolved, several mediators may be concerted for the development of renal lesions in the DOCS one-renin gene normotensive mouse model, such as high sodium intake, potassium depletion or hypokalemia, mineralocorticoids excess, intrarenal ischemia, vascular endothelial dysfunction, etc. This evidence concerns the gene REN and Hypokalemia.