Armanini D, Witzgall H, Wehling M, Kuhnle U, Weber P C
J Clin Endocrinol Metab. 1987 Jul;65(1):101-4. doi: 10.1210/jcem-65-1-101.
The number of mineralocorticoid-binding sites on mononuclear leukocytes and plasma aldosterone (aldo) concentrations were measured in patients with different types of primary hyperaldosteronism. Patients with unilateral adenoma and patients with bilateral adrenal hyperplasia had a significantly lower (P less than 0.001) mean number of binding sites for aldo [144 +/- 36 (+/- SD; n = 6) and 140 +/- 28 sites/cell (n = 4), respectively] compared with normal subjects (292 +/- 110 sites/cell; n = 25). In four patients with dexamethasone-suppressible hyperaldosteronism, mineralocorticoid-binding sites in mononuclear leukocytes were normal (291 +/- 108 sites/cell). In all patients undergoing surgery for unilateral adenoma, the receptors normalized 3 months after the operation. In two patients the reduction in receptors persisted for a short time after surgery even though the plasma aldo level had already normalized. We conclude that mineralocorticoid excess produces down-regulation of mineralocorticoid receptors, which, in turn, might contribute to the genesis of the aldo escape phenomenon.
对不同类型原发性醛固酮增多症患者的单核白细胞上盐皮质激素结合位点数量及血浆醛固酮(aldo)浓度进行了测定。与正常受试者(292±110个位点/细胞;n = 25)相比,单侧腺瘤患者和双侧肾上腺增生患者的aldo结合位点平均数量显著更低(P<0.001),分别为[144±36(±标准差;n = 6)和140±28个位点/细胞(n = 4)]。在4例地塞米松可抑制性醛固酮增多症患者中,单核白细胞中的盐皮质激素结合位点正常(291±108个位点/细胞)。在所有接受单侧腺瘤手术的患者中,术后3个月受体恢复正常。在2例患者中,尽管血浆aldo水平已经恢复正常,但术后受体减少仍持续了一段时间。我们得出结论,盐皮质激素过量会导致盐皮质激素受体下调,这反过来可能有助于醛固酮逃逸现象的发生。