Major findings demonstrate that in db/db mice, which are obese and have hyperaldosteronism and vascular MR hyperactivation: (i) hypercontractility is reduced by canrenoate and fasudil, (ii) upregulation of vascular RhoA/ROCK pro-contractile signaling is ameliorated by ROCK inhibition and MR blockade and is related to decreased cGMP-dependent PKG-1 activity, (iii) increased vascular expression of pro-inflammatory and pro-fibrotic mediators are downregulated by canreonate, and (iv) ROCK contributes to insulin resistance through MR-independent mechanisms. This evidence concerns the gene RHOA and hyperaldosteronism.