In the cardiovascular system aldosterone induces fibrosis and vascular dysfunction. However, in rabbit renal afferent arterioles (Uhrenholt et al. Circ Res 2003) and in rat aorta (Liu et al. Circulation 2003) aldosterone has a vasodilator effect that is seen within minutes, and is not inhibited by blockers of gene transcription, thus pointing to a non-genomic mechanism. Furthermore, this potentially beneficial effect is observed at low physiological concentrations of aldosterone (0.1–-10 pM). The effect is mediated by the mineralocorticoid receptor, and it involves heat shock protein 90, phosphatidylinositol (PI)-3 kinase, protein kinase B, endothelial nitric oxide synthase, and liberation of nitric oxide. Aldosterone also has the ability to elicit vasoconstriction in afferent arterioles through a pathway involving activation of phospholipase C and calcium influx in the vascular smooth muscles (Arima et al. JASN, 2003). Furthermore, aldosterone stimulates production of reactive oxygen species (ROS). It is proposed that in healthy individuals with a functioning NO system and ambient low production of ROS, aldosterone does not damage the blood vessels, while in conditions with endothelial dysfunction, such as congestive heart failure and hypertension, the negative effects of aldosterone will predominate (Skøtt et al. Pharmacol Ther, 2006).