Both (1) the increased aldosterone-MR mediated renal effects (leading to moderate sodium and water retention and excessive potassium excretion) and (2) aldosterone-MR and direct aldosterone mediated (MR-independent and non-genomic) vascular effects (contributing to e.g. vascular stiffening and endothelial dysfunction) result in arterial hypertension and, variably, hypokalemia [3–5]. This evidence concerns the gene NR3C2 and endothelial dysfunction.