Kocsis J F, Boyette M H, McIlroy P J, Carsia R V
Department of Cell Biology, University of Medicine and Dentistry of New Jersey-School of Osteopathic Medicine, Stratford 08084.
Gen Comp Endocrinol. 1994 Oct;96(1):108-21. doi: 10.1006/gcen.1994.1163.
The hormonal and cationic regulation of aldosterone production by freshly isolated turkey (Meleagris gallopavo) adrenal steroidogenic cells was investigated. Angiotensin II (AII), ACTH [human ACTH-(1-39)], and K+ stimulated aldosterone production in a concentration-dependent manner albeit these agents exhibited considerable differences in lag time for the significant stimulation of aldosterone production over basal production. By contrast, Ca2+ was without effect except at a high concentration (10 mM). Although ACTH was more efficacious than AII, it had about one-third the potency of AII for stimulating aldosterone production. However, ACTH potentiated the maximal aldosterone response to AII [maximal enhancement (+499%) at 3 x 10(-10) M ACTH]. Extracellular K+ was an absolute requirement for AII-induced aldosterone production (threshold concentration = 3 mM), and maximal enhancement (+200%) occurred with 5 mM (a physiological concentration). Although extracellular Ca2+ was not an absolute requirement for inducible aldosterone production, it enhanced AII-induced aldosterone production in a concentration-dependent manner [maximal enhancement (+727%) at 3 mM], albeit it did not alter the half-maximal steroidogenic concentration (EC50) of AII. Ca2+ also enhanced maximal ACTH-induced aldosterone production but to a lesser extent (+96% with 1 mM Ca2+). However, Ca2+ dramatically enhanced ACTH potency (ED50) (nearly 100 times at 1 mM Ca2+). The acute augmentation of AII-induced aldosterone production by ACTH, K+, and Ca2+ was not accompanied by increases in the cellular concentration and affinity of AII receptors, suggesting that the agents acted at intracellular loci distal to the AII receptor. Several aspects of the present study with isolated turkey adrenal steroidogenic cells differ markedly from those of studies with isolated chicken (Gallus gallus domesticus) adrenal steroidogenic cells and mammalian zona glomerulosa cells, thus suggesting interclass and intraclass differences in homeothermic vertebrate adrenal steroidogenic regulation.
研究了新鲜分离的火鸡(原鸡)肾上腺类固醇生成细胞中醛固酮生成的激素和阳离子调节。血管紧张素 II(AII)、促肾上腺皮质激素 [人促肾上腺皮质激素-(1-39)] 和 K+ 以浓度依赖的方式刺激醛固酮生成,尽管这些试剂在显著刺激醛固酮生成超过基础生成的滞后时间上表现出相当大的差异。相比之下,Ca2+ 没有作用,除非在高浓度(10 mM)时。虽然促肾上腺皮质激素比 AII 更有效,但它刺激醛固酮生成的效力约为 AII 的三分之一。然而,促肾上腺皮质激素增强了对 AII 的最大醛固酮反应 [在 3×10(-10) M 促肾上腺皮质激素时最大增强(+499%)]。细胞外 K+ 是 AII 诱导醛固酮生成的绝对必要条件(阈值浓度 = 3 mM),最大增强(+200%)发生在 5 mM(生理浓度)时。虽然细胞外 Ca2+ 不是诱导醛固酮生成的绝对必要条件,但它以浓度依赖的方式增强 AII 诱导的醛固酮生成 [在 3 mM 时最大增强(+727%)],尽管它没有改变 AII 的半最大类固醇生成浓度(EC50)。Ca2+ 也增强了最大促肾上腺皮质激素诱导的醛固酮生成,但程度较小(1 mM Ca2+ 时为 +96%)。然而,Ca2+ 显著增强了促肾上腺皮质激素的效力(ED50)(1 mM Ca2+ 时几乎增加了 100 倍)。促肾上腺皮质激素、K+ 和 Ca2+ 对 AII 诱导的醛固酮生成的急性增强并没有伴随着 AII 受体细胞浓度和亲和力的增加,这表明这些试剂作用于 AII 受体远端的细胞内位点。本研究中分离的火鸡肾上腺类固醇生成细胞的几个方面与分离的鸡(家鸡)肾上腺类固醇生成细胞和哺乳动物球状带细胞的研究有显著不同,因此表明恒温脊椎动物肾上腺类固醇生成调节存在类间和类内差异。