Morris D J, Souness G W, Brem A S, Oblin M E
Department of Pathology and Laboratory Medicine, The Miriam Hospital and Rhode Island Hospital, Brown University School of Medicine, Providence, RI 02906, USA.
Kidney Int. 2000 Apr;57(4):1370-3. doi: 10.1046/j.1523-1755.2000.00977.x.
: In Na+-transporting epithelial target tissues, such as mammalian kidney and the isolated toad bladder, glucocorticoids (GCs) do not normally elicit Na+ retention. In mammalian kidney, however, they do cause kaliuresis. The presence of 11beta-hydroxysteroid dehydrogenase isoform 2 (11beta-HSD2) in these target tissues inactivates the GCs, preventing them from accessing mineralocorticoid receptors (MRs) and stimulating Na+ transport.
: The usually observed Na+ retention elicited by the mineralocorticoid aldosterone was blunted when the GC corticosterone was coadministered along with aldosterone. However, when corticosterone was administered along with a 11beta-HSD2 inhibitor, a strong Na+ transport was elicited by an MR-mediated mechanism. 11-Dehydrocorticosterone also blunted aldosterone-elicited Na+ transport in these target tissues.
: 11beta-HSD2 appears to play two important roles in the epithelial target tissues, kidney and toad bladder. The first is to protect GC access to MR, and the second involves the product of the enzyme to regulate the magnitude of aldosterone-induced Na+ retention.
在钠转运上皮靶组织中，如哺乳动物肾脏和离体蟾蜍膀胱，糖皮质激素（GCs）通常不会引起钠潴留。然而，在哺乳动物肾脏中，它们会导致尿钾增多。这些靶组织中11β-羟基类固醇脱氢酶同工酶2（11β-HSD2）的存在会使GCs失活，阻止它们与盐皮质激素受体（MRs）结合并刺激钠转运。
当GC皮质酮与醛固酮共同给药时，通常观察到的由盐皮质激素醛固酮引起的钠潴留减弱。然而，当皮质酮与11β-HSD2抑制剂一起给药时，通过MR介导的机制会引发强烈的钠转运。11-脱氢皮质酮也会减弱这些靶组织中醛固酮引起的钠转运。
11β-HSD2似乎在肾脏和蟾蜍膀胱等上皮靶组织中发挥两个重要作用。第一个作用是保护GC与MR结合，第二个作用涉及该酶的产物调节醛固酮诱导的钠潴留程度。
