Webb C B, Szabo M, Frohman L A
Endocrinology. 1983 Oct;113(4):1191-6. doi: 10.1210/endo-113-4-1191.
Glucocorticoids and estrogens each affect GH secretion in vivo. The effects of corticosterone and estradiol (E2) were studied singly and in combination on GH secretion and cell content of primary cultures of rat adenohypophyseal cells grown in media containing intact or hormone-deficient serum. Secretion was measured under basal conditions and in response to maximally stimulatory doses of ectopic GH-releasing factor (E-GHRF) derived from a carcinoid tumor and dibutyryl cAMP [(DBcAMP) 10(-3) M]. Basal GH release measured over a 4-h period was suppressed by 40% (P less than 0.001) when hormone-deficient serum was substituted for normal serum in the growth media, and the stimulatory responses to DBcAMP and E-GHRF were markedly attenuated (P less than 0.001). The GH content of unstimulated cells was also decreased [29 +/- (SE) 7%, P less than 0.001]. The addition of corticosterone, 3 X 10(-8) M to 3 X 10(-6) M, to the 4-day growth media resulted in dose-related increases in basal and DBcAMP-stimulated GH release during the 4-h test period which was proportional to the increases in total cellular GH content. In contrast, corticosterone exposure caused a dose-related enhancement of E-GHRF-stimulated release above that accounted for by the increase in total GH content alone. Concomitant exposure to the releasing stimuli and corticosterone during a 4-h incubation, however, reduced the effects of the releasing stimuli. The addition of E2, 10(-10) M to 10(-8) M, during the 4-day growth period and/or the 4-h stimulation period did not affect the secretion of GH either basally or in response to the stimuli. E2 did increase the cell content of GH, but the effects were not additive to those of corticosterone. These studies indicate that long term (4-day) exposure to corticosterone increases net GH synthesis and E-GHRF-stimulated release, but that acute (4 h) exposure inhibits stimulated release. Although E2 also increases cellular content of GH, it exhibits no demonstrable direct effects on GH secretion or content in the presence of corticosterone.
糖皮质激素和雌激素均可在体内影响生长激素（GH）的分泌。研究了皮质酮和雌二醇（E2）单独及联合作用对在含完整血清或激素缺乏血清的培养基中培养的大鼠腺垂体细胞原代培养物中GH分泌和细胞含量的影响。在基础条件下以及对源自类癌肿瘤的异位生长激素释放因子（E - GHRF）和二丁酰环磷腺苷（[DBcAMP] 10⁻³ M）的最大刺激剂量作出反应时，对分泌进行了测定。当在生长培养基中用激素缺乏血清替代正常血清时，在4小时期间测得的基础GH释放被抑制了40%（P < 0.001），并且对DBcAMP和E - GHRF的刺激反应明显减弱（P < 0.001）。未受刺激细胞的GH含量也降低了[29 ± （标准误）7%，P < 0.001]。向4天的生长培养基中添加3×10⁻⁸ M至3×10⁻⁶ M的皮质酮，在4小时测试期内导致基础和DBcAMP刺激的GH释放呈剂量相关增加，这与总细胞GH含量的增加成比例。相比之下，皮质酮暴露导致E - GHRF刺激的释放比仅由总GH含量增加所解释的增加有剂量相关的增强。然而，在4小时孵育期间同时暴露于释放刺激物和皮质酮会降低释放刺激物的作用。在4天生长期间和/或4小时刺激期间添加10⁻¹⁰ M至10⁻⁸ M的E2，无论在基础状态下还是对刺激的反应中，均不影响GH的分泌。E2确实增加了GH的细胞含量，但这些作用与皮质酮的作用并非相加关系。这些研究表明，长期（4天）暴露于皮质酮会增加GH的净合成和E - GHRF刺激的释放，但急性（4小时）暴露会抑制刺激释放。虽然E2也会增加GH的细胞含量，但在存在皮质酮的情况下，它对GH分泌或含量没有明显的直接影响。
