Shibasaki T, Nakahara M, Shizume K, Kiyosawa Y, Suda T, Demura H, Kuwayama A, Kageyama N, Benoit R, Ling N
J Clin Endocrinol Metab. 1983 Feb;56(2):414-6. doi: 10.1210/jcem-56-2-414.
The response of pituitary adenomas obtained surgically from patients with Cushing's disease of Nelson's syndrome to synthetic ovine corticotropin-releasing factor (CRF), vasopressins, somatostatin-28, dexamethasone, 3-isobutylmethylxanthine or high [K+] was examined in vitro by measuring the amount of pro-opiomelanocortin (POMC)-derived peptides secreted into the culture medium. CRF did not stimulate the secretion of adrenocorticotropin-, beta-endorphin-, or gamma 3-melanotropin-like peptides from the pituitary adenomas at concentrations ranging from 1 x 10(-13) M to 1 x 10(-7) M whereas vasopressins, 3-isobutyrl-methylxanthine and high [K+] increased, while somatostatin-28 and dexamethasone suppressed, the secretion of these POMC-derived peptides. These findings suggest that either the pituitary ACTH-producing tumors have lost their receptors to CRF or their post-receptor mechanism to CRF is not functional.
通过测量分泌到培养基中的促肾上腺皮质激素原(POMC)衍生肽的量,在体外检测了从库欣病或纳尔逊综合征患者手术获取的垂体腺瘤对合成羊促肾上腺皮质激素释放因子(CRF)、血管加压素、生长抑素 - 28、地塞米松、3 - 异丁基甲基黄嘌呤或高[K⁺]的反应。在浓度范围为1×10⁻¹³ M至1×10⁻⁷ M时,CRF未刺激垂体腺瘤分泌促肾上腺皮质激素、β - 内啡肽或γ3 - 促黑素样肽,而血管加压素、3 - 异丁酰基甲基黄嘌呤和高[K⁺]增加了这些POMC衍生肽的分泌,而生长抑素 - 28和地塞米松则抑制了它们的分泌。这些发现表明,要么垂体产生促肾上腺皮质激素的肿瘤已经失去了对CRF的受体,要么其CRF的受体后机制不起作用。