抄録
The regulation of renal 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) gene expression is poorly understood. Inhibition of expression can result in hypertension. An example of this is in ectopic adrenocorticotropin (ACTH) syndrome (EAS). Inhibition of 11βHSD2 activity is suggested by the observed increased ratio of cortisol to cortisone in both plasma and urine. To investigate whether ACTH or ACTH-dependent steroids can modulate renal 11βIHSD2 gene expression we analysed renal 11βHSD2 mRNA levels after treatment with ACTH of 1H and 24H and demonstrated no change in the levels of gene expression. We have demonstrated in this study that the expression of 11βIHSD2 in the kidney is unaltered by ACTH. The reduced inactivation of cortisol by 11βIHSD2 observed in EAS is likely to be in part due to end product inhibition or substrate overload of the enzyme by endogenous substrates (cortisol, corticosterone, etc) rather than inhibition of 11βHSD2 at the transcriptional level by either ACTH or ACTH regulated steroids.
