Norbiato G, Bevilacqua M, Raggi U, Micossi P, Moroni C
J Clin Endocrinol Metab. 1977 Dec;45(6):1313-6. doi: 10.1210/jcem-45-6-1313.
Plasma Aldosterone (PA) response to metoclopramide (10 mg i.v.) was studied in 11 normal, 2 hypophysectomized subjects and in one patient with bilateral adrenal hyperplasia. All the subjects were kept on a normal sodium and potassium intake. Four normal subjects were pretreated with 1 mg of dexamethasone in order to inhibit endogenous ACTH. In all subjects metoclopramide elicited a prompt rise of PA comparable to that obtained with angiotensions or ACTH. No significant change of blood pressure, serum electrolytes, plasma renin activity, Plasma Cortisol (PC) was detected. The lack of PC response to metoclopramide and the PA increase in dexamethasone pretreated subjects rule out an ACTH mediated effect. The increase of PA in hypophysectomized subjects, in whom metoclopramide did not stimulate any prolactin release, rules out a prolactin mediated effect. Metoclopramide increases plasma aldosterone concentration probably via a direct action on the adrenal glomerular zone or throught another unknown mechanism.
在11名正常受试者、2名垂体切除受试者以及1名双侧肾上腺增生患者中,研究了血浆醛固酮(PA)对甲氧氯普胺(静脉注射10毫克)的反应。所有受试者均保持正常的钠和钾摄入量。4名正常受试者预先接受1毫克地塞米松治疗,以抑制内源性促肾上腺皮质激素(ACTH)。在所有受试者中,甲氧氯普胺引起PA迅速升高,与血管紧张素或ACTH引起的升高相当。未检测到血压、血清电解质、血浆肾素活性、血浆皮质醇(PC)有显著变化。地塞米松预处理的受试者中PC对甲氧氯普胺无反应且PA升高,排除了ACTH介导的效应。垂体切除受试者中PA升高,而甲氧氯普胺未刺激任何催乳素释放,排除了催乳素介导的效应。甲氧氯普胺可能通过对肾上腺球状带的直接作用或通过另一种未知机制增加血浆醛固酮浓度。