Protective and specificity-conferring mechanisms of mineralocorticoid action

Abstract

Several experiments using both the in vivo rat bioassay and the isolated toad bladder preparation have been reported that lend support to the hypothesis that the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD), in mineralocorticoid (MC) target tissues, acts as a “protective” mechanism that prevents endogenous glucocorticoids (GCs) from causing MC receptor-mediated effects on Na+ and K+. Additional experiments have also indicated that a second distinct protective mechanism exists that prevents endogenous MCs from eliciting excessive MC receptor-mediated Na+ retention. This second protective mechanism may involve steroid-metabolizing enzymes other than 11 beta-OHSD. Since the specific GC agonist, RU28362, can elicit Na+ retention and K+ secretion, it is possible that a third protective mechanism exists whereby renal 11 beta-OHSD prevents endogenous GCs from eliciting GC receptor-mediated effects on Na+ and K+.