Apparent mineralocorticoid excess, 11 beta hydroxysteroid dehydrogenase and aldosterone action - Closing one loop, opening another

The recent cloning of the human enzyme 11 beta hydroxysteroid dehydrogenase type 2 (11 beta HSD2), and the demonstration of point mutations or deletions in both familial and apparently sporadic cases of apparent mineralocorticoid excess (AME), underlines the importance of this enzyme in excluding glucocorticoids from mineralocorticoid receptors (MR). Although the sodium retention characteristic of AME can thus be explained by absent or very reduced (<10%) levels of renal 11 beta HSD2 activity, whether or not the enzymatic defect contributes to the elevated blood pressure by mechanisms other than sodium retention remains to be determined.