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血清素和L-5-羟色氨酸对大鼠血浆肾素活性的影响。

Effects of serotonin and L-5-hydroxytryptophan on plasma renin activity in rats.

作者信息

Barney C C, Threatte R M, Kikta D C, Fregly M J

出版信息

Pharmacol Biochem Behav. 1981 Jun;14(6):895-900. doi: 10.1016/0091-3057(81)90380-4.

Abstract

The effects of dipsogenic doses of l-5-hydroxytryptophan (5-HTP) and serotonin on plasma renin activity (PRA), blood pressure, and body temperature were determined in unanesthetized female rats. Both serotonin (2 mg/kg, s.c.) and 5-HTP (25 mg/kg, s.c.) induced six-fold increases in PRA measured 1 hr after drug administration. The central and peripheral decarboxylase inhibitor, benserazide (30 mg/kg, s.c.), as well as the peripheral decarboxylase inhibitor, carbidopa (6.5 mg/kg s.c.), prevented the increase in PRA associated with administration of 5-HTP. This suggests that 5-HTP must be converted to serotonin peripherally to increase PRA. At the doses used, serotonin decreased mean blood pressure and colonic temperature of unanesthetized rats while 5-HTP was without effect. The increase in PRA induced by 5-HTP does not appear, therefore, to be a response to either hypotension or a decrease in colonic temperature. Since 5-HTP must be converted to serotonin to initiate both a drinking response and an increase in PRA, the results suggest that the decrease in blood pressure and colonic temperature following administration of serotonin may not be important in induction of the drinking response and the increase in PRA. The mechanism by which activation of the renin-angiotensin system occurs following peripheral administration of either 5-HTP or serotonin remains for further study.

摘要

在未麻醉的雌性大鼠中,测定了致渴剂量的L-5-羟色氨酸(5-HTP)和血清素对血浆肾素活性(PRA)、血压和体温的影响。血清素(2mg/kg,皮下注射)和5-HTP(25mg/kg,皮下注射)在给药后1小时测定时均使PRA增加了6倍。中枢和外周脱羧酶抑制剂苄丝肼(30mg/kg,皮下注射)以及外周脱羧酶抑制剂卡比多巴(6.5mg/kg,皮下注射)可防止与5-HTP给药相关的PRA升高。这表明5-HTP必须在外周转化为血清素才能增加PRA。在所使用的剂量下,血清素降低了未麻醉大鼠的平均血压和结肠温度,而5-HTP则无此作用。因此,5-HTP诱导的PRA升高似乎不是对低血压或结肠温度降低的反应。由于5-HTP必须转化为血清素才能引发饮水反应和PRA升高,结果表明血清素给药后血压和结肠温度的降低在诱导饮水反应和PRA升高方面可能并不重要。外周给予5-HTP或血清素后肾素-血管紧张素系统激活的机制仍有待进一步研究。

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