Aldosterone has actions far beyond its role as a renal regulator of sodium reabsorption and broader mechanisms of action than simply a transcriptional regulator. Aldosterone has a number of vascular effects including regulation of vascular reactivity and vascular growth/development. Aldosterone‐mediated effects on vascular reactivity reflect a balance between its endothelial‐dependent vasodilator effects and its direct smooth muscle vasoconstrictor effects. The endothelial vasodilator effects of aldosterone are mediated by phosphoinositide 3 kinase (PI3K)‐dependent nitric oxide synthase (NOS) activation. GPER is a recently recognized G protein coupled receptor (GPCR) that is activated by steroid hormones. It was first recognized as the GPCR mediating the rapid effects of estrogens. GPER activation also mediates at least some of aldosterone's vascular effects in smooth muscle and in endothelial cells. In vascular endothelial cells aldosterone activation of GPER mediates vasodilation. In contrast endothelial MR activation has been linked to enhanced vasoconstrictor and/or impaired vasodilator responses. This article is protected by copyright. All rights reserved.