Glucocorticoids action in etiology of hypertension

Abstract

Glucocorticoids (GKS), among which cortisol (F) is the most important factor, have various metabolic functions. They regulate glucose levels and influence proteins and lipids metabolism. Higher secretion of F, its changed metabolism or higher sensitivity of cells or tissues to F might be a source of metabolic disorders and many diseases, inter alia arterial hypertension. The key enzyme in F metabolism is 11b-hydroxysteroid dehydrogenase, which catalyzes the interconversion of F and inactive cortisone. The isoform 2 of that enzyme (11β-HSD2) is responsible for mineralocorticoid receptor’s protection from F. Disturbances in activity of 11β-HSD2, for example in apparent mineralocorticoid excess, lead to mineralocorticoid receptor activation by F, water retention and finally to hypertension. The influence of GKS on nitric oxide (NO) synthesis is another possible mechanism of hypertensive action of GKS. Decrease of NO levels may be an effect of inhibition of expression of nitric oxide synthase isoform 2 and 3, lack of enzyme co-factor or the substrate for NO synthesis. The paper summarises data considering GKS influence on pathomechanism of arterial hypertension.
Arterial Hypertension 2010, vol. 14, no 3, pages 208-215