Rolland P H, Rolland A M, Benkoel L, Toga M
Mol Cell Endocrinol. 1981 May;22(2):179-93. doi: 10.1016/0303-7207(81)90090-3.
In bovine adrenal cortex cells, dispersed without preferential loss of cells, we investigated (1) whether endogenous prostaglandins (PGs) are involved in ACTH-induced adrenal steroidogenesis, and (2) the steroidogenic effects of PGs and PG analogs. Free cells produced considerable amounts of PGE2, whereas only minute quantities of PGF2 alpha and PGA1 were synthesized. PGE2 synthesis, however, was not significantly increased when ACTH elicited a steroidogenic response in free cells. High concentrations of PG-synthesis inhibitors such as indomethacin affected both PG synthesis and steroidogenesis, whereas intermediate concentrations (10(-6) M) inhibited production of both PGE2 and aldosterone even after cAMP and cortisol response to ACTH had returned to normal values. It is concluded that endogenous PGE2 is not a link in the acute mechanism of action of trophic hormones in which cAMP is involved. Of the prostanoid structures, PGs of the E series were the most potent stimulating agents of cortisol production, although less active than ACTH. On the other hand, PGA1 induced an ACTH-like aldosterone synthesis. PGE2 was less active, and other prostanoid structures were without effect on aldosterone production. It is suggested that in pathological circumstances, PGA1 regulates aldosterone production and PGE2 increases both aldosterone and cortisol production.
在牛肾上腺皮质细胞中,细胞分散良好且无细胞选择性丢失的情况下,我们研究了:(1)内源性前列腺素(PGs)是否参与促肾上腺皮质激素(ACTH)诱导的肾上腺类固醇生成;(2)PGs和PG类似物的类固醇生成作用。游离细胞产生大量的前列腺素E2(PGE2),而仅合成微量的前列腺素F2α(PGF2α)和前列腺素A1(PGA1)。然而,当ACTH在游离细胞中引发类固醇生成反应时,PGE2的合成并未显著增加。高浓度的PG合成抑制剂如吲哚美辛会影响PG合成和类固醇生成,而中等浓度(10⁻⁶ M)即使在对ACTH的环磷酸腺苷(cAMP)和皮质醇反应恢复到正常水平后,仍会抑制PGE2和醛固酮的产生。结论是,内源性PGE2不是涉及cAMP的促营养激素急性作用机制中的一个环节。在前列腺素结构中,E系列前列腺素是皮质醇产生的最有效刺激剂,尽管活性低于ACTH。另一方面,PGA1诱导类似ACTH的醛固酮合成。PGE2活性较低,其他前列腺素结构对醛固酮产生无影响。提示在病理情况下,PGA1调节醛固酮产生,PGE2增加醛固酮和皮质醇的产生。