Morris D J, Souness G W
Am J Physiol. 1992 Nov;263(5 Pt 2):F759-68. doi: 10.1152/ajprenal.1992.263.5.F759.
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+.
已有多项使用体内大鼠生物测定法和离体蟾蜍膀胱制备法的实验报道，这些实验支持了以下假说：在盐皮质激素（MC）靶组织中，11β-羟类固醇脱氢酶（11β-OHSD）作为一种“保护”机制，可防止内源性糖皮质激素（GCs）引起MC受体介导的对钠和钾的作用。另外的实验还表明，存在第二种不同的保护机制，可防止内源性MCs引发过度的MC受体介导的钠潴留。这种第二种保护机制可能涉及11β-OHSD以外的类固醇代谢酶。由于特异性GC激动剂RU28362可引起钠潴留和钾分泌，因此可能存在第三种保护机制，即肾脏中的11β-OHSD可防止内源性GCs引起GC受体介导的对钠和钾的作用。
