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左旋多巴对人肾素-血管紧张素-醛固酮系统的抑制作用:有无脑外多巴脱羧酶抑制的情况

Inhibition of the renin-angiotensin-aldosterone system by L-dopa with and without inhibition of extracerebral dopa decarboxylase in man.

作者信息

Barbieri C, Caldara R, Ferrari C, Crossignani R M, Recchia M

出版信息

Clin Sci (Lond). 1981 Aug;61(2):187-90. doi: 10.1042/cs0610187.

Abstract
  1. The present study was undertaken to investigate the possibility that central nervous system mono-aminergic pathways may play a role in the control of the renin-angiotensin-aldosterone system in man. 2. Eight normal subjects received in a randomized order placebo, L-dopa (500 mg, orally) and L-dopa (100 mg, orally) plus carbidopa (35 mg, orally) after pretreatment with carbidopa (50 mg every 6 h for four doses). 3. L-Dopa administration elicited a significant fall in plasma renin activity (PRA) (P less than 0.01 at 120, 150 and 180 min) and in plasma aldosterone levels (P less than 0.05 at 90, 120, 150 and 180 min); L-dopa plus carbidopa induced a decrease in PRA (P less than 0.05 at 120 and 150 min, P less than 0.01 at 180 min) and in plasma aldosterone concentration (P less than 0.05 at 30 and 60 min, P less than 0.01 at 90 and 120 min), in comparison with placebo administration; between-drugs analysis revealed no difference in the decreases in PRA and plasma aldosterone levels induced by the two regimens. 4. Since L-dopa, as well as L-dopa plus carbidopa, has been shown to augment catecholamine levels in the brain of various animal species, the present data suggest that in man PRA and plasma aldosterone concentration might be inhibited by increased central nervous system catecholamine levels.
摘要
  1. 本研究旨在探讨中枢神经系统单胺能通路可能在人类肾素 - 血管紧张素 - 醛固酮系统的调控中发挥作用的可能性。2. 八名正常受试者在接受卡比多巴(每6小时50毫克,共四剂)预处理后,按随机顺序接受安慰剂、左旋多巴(口服500毫克)和左旋多巴(口服100毫克)加卡比多巴(口服35毫克)。3. 给予左旋多巴后,血浆肾素活性(PRA)显著下降(在120、150和180分钟时P<0.01),血浆醛固酮水平也下降(在90、120、150和180分钟时P<0.05);与给予安慰剂相比,左旋多巴加卡比多巴导致PRA下降(在120和150分钟时P<0.05,在180分钟时P<0.01),血浆醛固酮浓度下降(在30和60分钟时P<0.05,在90和120分钟时P<0.01);两种给药方案引起的PRA和血浆醛固酮水平下降的药物间分析显示无差异。4. 由于已证明左旋多巴以及左旋多巴加卡比多巴可提高多种动物大脑中的儿茶酚胺水平,目前的数据表明,在人类中,中枢神经系统儿茶酚胺水平升高可能会抑制PRA和血浆醛固酮浓度。

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