Suppr超能文献

血清素和5-羟色氨酸对麻醉大鼠血压和肾血流量的影响

Serotonin and 5-hydroxytryptophan on blood pressure and renal blood flow in anesthetized rats.

作者信息

Ding X R, Stier C T, Itskovitz H D

机构信息

Department of Medicine, New York Medical College, Valhalla 10595.

出版信息

Am J Med Sci. 1989 May;297(5):290-3. doi: 10.1097/00000441-198905000-00004.

Abstract

The effects of exogenous (injected) serotonin on mean blood pressure and renal blood flow in male Sprague-Dawley rats were compared with the effects of enhanced endogenous serotonin, accomplished by injections of 5-hydroxytryptophan (5-HTP). Responses were evaluated with and without carbidopa, which blocks peripheral conversion of 5-HTP to serotonin, and with and without indomethacin to assess the contribution of prostanoids. Both serotonin (0.25-1.0 micrograms) and 5-HTP (50-200 micrograms) decreased blood pressure and renal blood flow and increased renal vascular resistance in dose-dependent fashion. Hypotensive responses with both agents were greater after arterial injections into the aortic arch than after intravenous injections (into the jugular vein). Carbidopa had no significant effects on responses to serotonin but ablated the ability of 5-HTP to increase renal vascular resistance and decrease renal blood flow. Carbidopa did not alter the hypotensive action of 5-HTP. Indomethacin had no significant effect on responses to serotonin or 5-HTP. These results support a direct renal vasoconstrictor effect for exogenous and endogenously formed serotonin and a hypotensive effect probably arising in the central nervous system.

摘要

将外源性(注射)血清素对雄性斯普拉格-道利大鼠平均血压和肾血流量的影响,与通过注射5-羟色氨酸(5-HTP)增强内源性血清素的影响进行了比较。在有和没有卡比多巴(其可阻断5-HTP外周转化为血清素)的情况下,以及在有和没有吲哚美辛的情况下评估反应,以评估前列腺素的作用。血清素(0.25 - 1.0微克)和5-HTP(50 - 200微克)均以剂量依赖性方式降低血压和肾血流量,并增加肾血管阻力。两种药物经主动脉弓动脉注射后的降压反应均比经静脉注射(颈静脉)后的更大。卡比多巴对血清素反应无显著影响,但消除了5-HTP增加肾血管阻力和降低肾血流量的能力。卡比多巴并未改变5-HTP的降压作用。吲哚美辛对血清素或5-HTP的反应无显著影响。这些结果支持外源性和内源性生成的血清素具有直接的肾血管收缩作用,以及可能在中枢神经系统产生的降压作用。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验