Sommers D K, Meyer E C, van Wyk M
Department of Pharmacology, University of Pretoria, South Africa.
Res Exp Med (Berl). 1991;191(6):423-7. doi: 10.1007/BF02576697.
This study examines the contribution of the serotonergic system to metoclopramide-induced aldosterone secretion. Six normal male volunteers, at 13 h, 9 h, and 2 h before the i.v. bolus of 10 mg metoclopramide, received the following pre-treatments in a single-blind cross-over randomized sequence: fluoxetine 20 mg, metergoline 6 mg, pizotifen 0.5 mg, or methysergide 2 mg. One regimen consisted of metoclopramide alone. Pizotifen and fluoxetine pre-treatment increased metoclopramide-induced aldosterone secretion significantly after 15 min, for the duration in the case of fluoxetine, and up to 90 min with pizotifen. The increase with metergoline was never significant, while methysergide had a negligible influence. Serotonin is postulated to play an intermediary role in acetylcholine-facilitated aldosterone release. The mechanism of fluoxetine-mediated serotonin increase is a re-uptake inhibition and that of pizotifen is suggested to be the elimination of an auto-inhibitory mechanism.
本研究考察了5-羟色胺能系统对甲氧氯普胺诱导的醛固酮分泌的作用。6名正常男性志愿者在静脉推注10 mg甲氧氯普胺前13小时、9小时和2小时，按单盲交叉随机顺序接受以下预处理：氟西汀20 mg、麦角苄酯6 mg、苯噻啶0.5 mg或甲基麦角新碱2 mg。一种方案仅为甲氧氯普胺。苯噻啶和氟西汀预处理在15分钟后显著增加了甲氧氯普胺诱导的醛固酮分泌，氟西汀的作用持续存在，而苯噻啶的作用持续长达90分钟。麦角苄酯的增加从未显著，而甲基麦角新碱的影响可忽略不计。推测5-羟色胺在乙酰胆碱促进的醛固酮释放中起中介作用。氟西汀介导的5-羟色胺增加的机制是再摄取抑制，而苯噻啶的机制被认为是消除自身抑制机制。
