CORTICOSTERONE METABOLISM AND MEMBRANE-TRANSPORT

The mammalian kidney metabolizes virtually all of the steroid hormones . Corticosterone receptors have been found in the cortical collecting tubule, and at least four metabolites of the hormone have been identif ied in rat renal tissue and urine. The biologic activity of these meta bolites is not completely known. In this study, we examined the functi onal effects of three of the metabolites of corticosterone on membrane transport in toad and turtle bladders; we also analyzed the oxidoredu ctase pathways for corticosterone metabolism. In the toad bladder, max imal water flow (vasopressin- and cyclic AMP-stimulated) was unaffecte d by corticosterone, 11-dehydro-20-dihydrocorticosterone (metabolite I ) and 11-dehydrocorticosterone (metabolite IV); maximal water flow was significantly inhibited by 20-dihydrocorticosterone (metabolite II). Sodium transport in the toad bladder was stimulated by corticosterone, 11-dehydrocorticosterone and 20-dihydrocorticosterone. Analysis of th e oxidoreductase pathways in this tissue revealed that most of the cor ticosterone was oxidized to 11-dehydrocorticosterone, a biologically a ctive compound; 11-dehydrocorticosterone was further metabolized to 11 -dehydro-20-dihydrocorticosterone, a biologically inactive compound. O nly 6% of the parent compound was converted to 20-dihydrocorticosteron e. In the turtle bladder, none of the metabolites tested altered hydro gen ion secretion over the time period studied; no significant biotran sformation of corticosterone occurred in this tissue. As the metabolit es of corticosterone found in toad bladder are the same as those ident ified in mammalian tissues, our studies suggest that some of them may be important modulators of sodium and water transport in the distal ne phron. Our data further suggest that these compounds are likely not in volved in the regulation of urinary acidification.