Renal interstitial corticosterone and 11-dehydrocorticosterone in conscious rats

cies in the conversion between active and inactive glucocorticoids in the kidney can lead to hypertension. However, the significance of glucocorticoid metabolism in specific kidney regions in vivo is not clear, possibly in part due to the difficulty in measuring glucocorticoid levels in kidney regions in vivo. We used microdialysis techniques to sample renal interstitial fluid from conscious rats. The levels of corticosterone (active) and 11-dehydrocorticosterone (inactive) were analyzed by liquid chromatography-tandem mass spectrometry. Direct infusion of the 11-hydroxysteroid dehydrogenase (11-HSD) inhib-itor carbenoxolone into the renal medulla induced hypertension, and significantly increased corticosterone levels and the corticosterone/ 11-dehydrocorticosterone ratio, an index of 11-HSD activity, in the renal medullary microdialysate, but not in urine or the plasma. Further characterization of conscious, untreated rats (n 13–16) indicated that corticosterone concentrations (ng/ml) were 0.8 0.1, 1.0 0.1