The cardiovascular system is now recognized as an important mineralocortico
id target. All components required for specific and selective aldosterone e
ffects are present in the cardiovascular system. Mineralocorticoid receptor
s (MR) are expressed in the heart and large blood vessels together with the
11 beta-hydroxysteroid dehydrogenase type II, which ensures the enzymatic
protection of MR against glucocorticoids. The recent description of local v
ascular and cardiac aldosterone biosynthesis strongly supports an autocrine
/paracrine hormonal action. Establishment of transgenic mice models of targ
eted overexpression of the mineralocorticoid receptor should facilitate new
insights into the molecular and cellular mechanisms of aldosterone actions
in the cardiovascular system.