Matsuoka H, Tan S Y, Mulrow P J
Prostaglandins. 1980 Feb;19(2):291-8. doi: 10.1016/0090-6980(80)90027-1.
To elucidate the role of prostaglandins in adrenal steroidogenesis, we studied aldosterone and corticosterone responses to 3 x 10(-8) M--3 x 10(-4) M of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), prostacyclin (PGI2), and arachidonic acid (AA) in collagenase dispersed rat adrenal capsular and decapsular cells. Whereas adrenocorticotrophic hormone (ACTH) and angiotensin II (AII) stimulated aldosterone production in capsular cells and ACTH stimulated corticosterone production in decapsular cells in a dose dependent fashion, aldosterone and corticosterone production were not stimulated significantly by PGE2, PGF2 alpha, PGI2, and AA. Although preincubation of dispersed adrenal cells with indomethacin (3 x 10(-5) M) markedly inhibited PGE2 synthesis, ACTH- and AII-stimulated aldosterone production and ACTH-stimulated corticosterone production were not attenuated despite prostaglandin blockade. These results indicate that prostaglandins are unlikely to play an important role in adrenal steroidogenesis.
为阐明前列腺素在肾上腺类固醇生成中的作用，我们研究了在胶原酶分散的大鼠肾上腺被膜和去被膜细胞中，醛固酮和皮质酮对3×10⁻⁸M - 3×10⁻⁴M前列腺素E2（PGE2）、前列腺素F2α（PGF2α）、前列环素（PGI2）和花生四烯酸（AA）的反应。促肾上腺皮质激素（ACTH）和血管紧张素II（AII）以剂量依赖方式刺激被膜细胞中醛固酮的产生，ACTH刺激去被膜细胞中皮质酮的产生，而PGE2、PGF2α、PGI2和AA并未显著刺激醛固酮和皮质酮的产生。尽管用吲哚美辛（3×10⁻⁵M）预孵育分散的肾上腺细胞可显著抑制PGE2的合成，但尽管前列腺素被阻断，ACTH和AII刺激的醛固酮产生以及ACTH刺激的皮质酮产生并未减弱。这些结果表明，前列腺素不太可能在肾上腺类固醇生成中起重要作用。
