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γ-氨基丁酸和牛磺酸可拮抗血管紧张素II和肾素对大鼠水盐摄入及血压的中枢作用。

Gamma-aminobutyric acid and taurine antagonize the central effects of angiotensin II and renin on the intake of water and salt, and on blood pressure in rats.

作者信息

Abe M, Tokunaga T, Yamada K, Furukawa T

机构信息

Department of Pharmacology, School of Medicine, Fukuoka University, Japan.

出版信息

Neuropharmacology. 1988 Mar;27(3):309-18. doi: 10.1016/0028-3908(88)90049-4.

Abstract

Antagonism by neuro-amino acids of the central effects of angiotensin II and renin in rats was investigated. Angiotensin II (100 ng), injected into the preoptic area, stimulated the intake of water but not salt, to a lesser extent and with a shorter duration as compared with that induced by renin (5 mU), injected into the preoptic area. This angiotensin II-induced intake of water was markedly inhibited by [Sar1, Ile8]-angiotensin II, an angiotensin II receptor antagonist, but not by captopril, an angiotensin-converting enzyme inhibitor, previously administered through the same cannula. The angiotensin II-induced intake of water was also inhibited in a dose-dependent manner by gamma-aminobutyric acid (GABA) (50-100 micrograms), muscimol, a GABA agonist, (100-200 ng), taurine (100-200 micrograms) and hypotaurine (100-200 micrograms), administered into the cerebroventricle and by GABA (5-10 micrograms), muscimol (10-20 ng) and taurine (10-20 micrograms) injected into the preoptic area in smaller doses. Renin (5 mU), injected into the preoptic area, elicited a marked increase in the intake of water and salt, which lasted for about 3 days. The effect of renin was inhibited by [Sar1, Ile8]-angiotensin II (10 micrograms) and was eliminated by captopril (25 micrograms) injected into the preoptic area. This effect of renin was not influenced by the peripheral administration of captopril. The effect of renin was also inhibited by GABA, muscimol or taurine injected into the cerebroventricle, in larger doses, or into the preoptic area in smaller doses.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了神经氨基酸对大鼠血管紧张素II和肾素中枢效应的拮抗作用。将血管紧张素II(100纳克)注入视前区,可刺激水的摄入,但不刺激盐的摄入,与注入视前区的肾素(5毫单位)相比,程度较轻且持续时间较短。这种血管紧张素II诱导的水摄入受到血管紧张素II受体拮抗剂[Sar1,Ile8]-血管紧张素II的显著抑制,但不受先前通过同一套管给药的血管紧张素转换酶抑制剂卡托普利的抑制。血管紧张素II诱导的水摄入也受到脑室注射的γ-氨基丁酸(GABA)(50 - 100微克)、GABA激动剂蝇蕈醇(100 - 200纳克)、牛磺酸(100 - 200微克)和亚牛磺酸(100 - 200微克)以及较小剂量注入视前区的GABA(5 - 10微克)、蝇蕈醇(10 - 20纳克)和牛磺酸(10 - 20微克)的剂量依赖性抑制。将肾素(5毫单位)注入视前区,可引起水和盐摄入量的显著增加,持续约3天。肾素的作用受到注入视前区的[Sar1,Ile8]-血管紧张素II(10微克)的抑制,并被注入视前区的卡托普利(25微克)消除。肾素的这种作用不受卡托普利外周给药的影响。肾素的作用也受到较大剂量注入脑室或较小剂量注入视前区的GABA、蝇蕈醇或牛磺酸的抑制。(摘要截取自250字)

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