Leboulenger F, Benyamina M, Delarue C, Netchitaïlo P, Saint-Pierre S, Vaudry H
Groupe de Recherche en Endocrinologie Moléculaire, UA C.N.R.S. 650, Unité Alliée à l'INSERM, Faculté des Sciences, Université de Rouen, Mont-Saint-Aignan, France.
Brain Res. 1988 Jun 21;453(1-2):103-9. doi: 10.1016/0006-8993(88)90147-3.
The adrenocortical cells of frog interrenal (adrenal) tissue are controlled by multiple factors. Recently, we have shown that corticosteroidogenesis is stimulated by acetylcholine released from splanchnic nerve terminals as well as by serotonin and vasoactive intestinal peptide (VIP) which are both contained in chromaffin cells. Since these 3 putative neuroregulators are known to interact with each other on various target organs, we have investigated possible coordinate actions of acetylcholine, serotonin and VIP on adrenal steroid production, using a perifusion system technique for frog interrenal tissue. Simultaneous infusion of submaximal doses of VIP (10(-5) M) and acetylcholine (5 X 10(-5) M) induced stimulations of corticosteroids (corticosterone and aldosterone) which were strictly additive. When VIP (10(-5) M) and serotonin (5 X 10(-6) M) were infused together, a potentiation of the individual responses was observed. In contrast, concomitant infusion of acetylcholine (5 X 10(-5) M) and serotonin (5 X 10(-6) M) caused a total blockage of the stimulatory effect of serotonin. Muscarine (10(-5) M) caused a similar blockade of the response of adrenocortical cells to serotonin while nicotine (5 X 10(-5) M) did not alter the stimulatory effect of serotonin. The inhibitory effect of acetylcholine on serotonin-induced steroidogenesis was antagonized by atropine (10(-5) M). Thus, acetylcholine appears to block the corticotropic action of serotonin by interacting with typical muscarinic receptors. Taken together our results indicate that 3 of the neuroregulators which participate in the control of adrenal steroidogenesis, namely acetylcholine, serotonin and VIP, may interact on their target cell to modulate the activity of their congeners.(ABSTRACT TRUNCATED AT 250 WORDS)
青蛙肾上腺（肾上腺皮质）组织的肾上腺皮质细胞受多种因素控制。最近，我们发现，发自内脏神经末梢释放的乙酰胆碱以及嗜铬细胞中所含的血清素和血管活性肠肽（VIP）均可刺激皮质类固醇生成。由于已知这三种假定的神经调节因子在各种靶器官上会相互作用，因此我们使用青蛙肾上腺组织的灌流系统技术，研究了乙酰胆碱、血清素和VIP对肾上腺类固醇生成可能的协同作用。同时输注亚最大剂量的VIP（10⁻⁵M）和乙酰胆碱（5×10⁻⁵M）可刺激皮质类固醇（皮质酮和醛固酮）生成，且这种刺激严格呈相加性。当一起输注VIP（10⁻⁵M）和血清素（5×10⁻⁶M）时，可观察到个体反应增强。相反，同时输注乙酰胆碱（5×10⁻⁵M）和血清素（5×10⁻⁶M）会导致血清素刺激作用完全受阻。毒蕈碱（10⁻⁵M）对肾上腺皮质细胞对血清素的反应有类似的阻断作用，而尼古丁（5×10⁻⁵M）不会改变血清素的刺激作用。乙酰胆碱对血清素诱导的类固醇生成的抑制作用可被阿托品（10⁻⁵M）拮抗。因此，乙酰胆碱似乎通过与典型的毒蕈碱受体相互作用来阻断血清素的促肾上腺皮质作用。综合我们的结果表明，参与肾上腺类固醇生成控制的三种神经调节因子，即乙酰胆碱、血清素和VIP，可能在其靶细胞上相互作用，以调节同类物质的活性。（摘要截取自250词）
