Hindawi R K, Al-Dujaili E A, Padfield P L
Prostaglandins Leukot Med. 1985 Nov;20(2):121-8. doi: 10.1016/0262-1746(85)90002-2.
The effect of PGE2 and PGA1 on aldosterone and corticosterone biosynthesis by isolated perfused rat zona glomerulosa cells has been studied. Incremental doses of each of the prostaglandins tested produced a progressive rise in aldosterone (3-4 fold increase for PGE2 and 2-3 fold increase for PGA1) and corticosterone (4-8 fold for PGE2 and 2-4 fold for PGA1). The cyclo-oxygenase inhibitors indomethacin and meclofenamate however produced no effect on basal steroidogenesis. PGE2 produced a marked potentiation of angiotensin II-induced aldosterone secretion (45.7 +/- 13.6 to 144.3 +/- 19.4 pg/ml with angiotensin II alone and 78.4 +/- 16.6 to 269.9 +/- 39.5 pg/ml with angiotensin II + PGE2). In contrast, there was no effect of PGE2 on ACTH or serotonin-induced aldosterone secretion. These data show that PGE2 and PGA1 can directly stimulate rat adrenal steroidogenesis and suggest that PGE2 may play a role in mediating angiotensin II-induced aldosterone secretion by rat zone glomerulosa cells.
研究了前列腺素E2（PGE2）和前列腺素A1（PGA1）对离体灌注的大鼠肾小球带细胞醛固酮和皮质酮生物合成的影响。所测试的每种前列腺素的递增剂量均使醛固酮（PGE2增加3 - 4倍，PGA1增加2 - 3倍）和皮质酮（PGE2增加4 - 8倍，PGA1增加2 - 4倍）逐渐升高。然而，环氧化酶抑制剂吲哚美辛和甲氯芬那酸对基础类固醇生成没有影响。PGE2显著增强了血管紧张素II诱导的醛固酮分泌（单独使用血管紧张素II时为45.7±13.6至144.3±19.4 pg/ml，血管紧张素II + PGE2时为78.4±16.6至269.9±39.5 pg/ml）。相比之下，PGE2对促肾上腺皮质激素（ACTH）或血清素诱导的醛固酮分泌没有影响。这些数据表明，PGE2和PGA1可直接刺激大鼠肾上腺类固醇生成，并提示PGE2可能在介导血管紧张素II诱导的大鼠肾小球带细胞醛固酮分泌中起作用。
