In double-transgenic hypertensive mouse models, increased salt intake “exacerbated” Ang II-induced kidney damage mediated by this Rac1-MR axis, which manifested as glomerulosclerosis and proteinuria, a process that was prevented by both Rac1 inhibitors and MR antagonists, but not simply by lowering blood pressure [23]. Here, RAC1 is linked to Nephropathy.