Metoclopramide에 의한 혈장 Aldosterone치 증가작용에 대한 Dopamine성 영향

Title
Metoclopramide에 의한 혈장 Aldosterone치 증가작용에 대한 Dopamine성 영향
Other Titles
Dopaminergic Influence on the Increase of Hasma Aldosterone level by Metoclopramide in Mice
Authors
김수경
Issue Date
1989
Publisher
Keimyung University School of Medicine
Citation
Keimyung Medical Journal, Vol.8(1) : 104~112, 1989
Abstract
The biosynthesis and secretion of aldosterone in adrenal gland is well known to be regulated by several factors. Especially; angiotensin II; ACTH; extracellular potssium are dominent factors. Recent studies suggest that dopamine may be a physiological regulator of aldosterone secretion. Therefore; the present study was undertaken to examine whether change of aldosterone response on metoclopramide is mediated by dopaminergic receptor. The results obtained were summarized as follows; 1. The plasma aldosterone level was significantly increased by metoclopramide( lOmg/kg) and ACTH(5u7kg); but not affected by dopamine (5mg/kg). 2. The metoclopramide-induced increase of plasma aldosterone level was significantly augmented by ACTH; but inhibited by dopamine. The ACTH-induced increase of plasma aldosterone level was slightly inhibited by dopamine. 3. The plasma sodium concentration was slightly increased by metoclopramide and ACTH; but not affected by dopamine. 4. The metoclopramide or ACTH-induced increase of plasma sodium concentration was inhibited by dopamine. The metoclopramide-induced increase of plasma sodium concentration was not affected by ACTH. 5. The plasma potassium concentration was slightly decreased by metoclopramide and ACTH; but significantly increased by dopamine. 6. The metoclopramide-induced decrease of plasma potassium concentration was not affected by ACTH; but significantly inhibited by dopamine. The ACTH-induced decrease of plasma potassium concentration was slightly inhibited by dopamine. The above results suggest that the increase of aldosterone secretion by metoclopramide is presumably mediated by dopaminergic receptor.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/2586
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학술지 > 1989
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