慢性尼古丁处理可增强大鼠对花生四烯酸的降压反应。
Chronic nicotine treatment enhances the depressor responses to arachidonic acid in the rat.
作者信息
Hui S C, Ogle C W
机构信息
Department of Pharmacology, Faculty of Medicine, University of Hong Kong.
出版信息
Pharmacology. 1991;42(5):257-61. doi: 10.1159/000138806.
The depressor responses to intravenous injections of arachidonic acid, prostacyclin (PGI2), prostaglandin E2 (PGE2) and sodium nitroprusside were studied in chronically nicotine-treated rats. Arachidonic acid, PGI2, PGE2 and sodium nitroprusside decreased the diastolic blood pressure dose-dependently in the control animals. The vasodepressor effect of arachidonic acid was significantly enhanced in rats given nicotine 5 and 25 micrograms/ml in their drinking water for 10 days but remained unchanged in the animals treated with 1 microgram/ml nicotine for 10 days or given 1 mg/kg i.v. nicotine 10 min before administration of arachidonic acid. Indometacin abolished arachidonic-acid-induced depressor responses in both the control and nicotine-treated rats. Hypotension induced by PGI2, PGE2 and sodium nitroprusside was of similar magnitude in the control and nicotine-treated animals. It is suggested that the enhancement by chronic nicotine treatment of depressor responses to arachidonic acid could be due to changes in the formation and/or removal of its vaso-active metabolites (i.e. prostacyclin and/or thromboxane A2).
在长期接受尼古丁处理的大鼠中，研究了静脉注射花生四烯酸、前列环素（PGI2）、前列腺素E2（PGE2）和硝普钠后的降压反应。在对照动物中，花生四烯酸、PGI2、PGE2和硝普钠均剂量依赖性地降低舒张压。在饮用含5微克/毫升和25微克/毫升尼古丁的水10天的大鼠中，花生四烯酸的血管舒张降压作用显著增强，但在饮用含1微克/毫升尼古丁的水10天的动物中或在注射花生四烯酸前10分钟静脉注射1毫克/千克尼古丁的动物中，该作用保持不变。吲哚美辛消除了对照大鼠和尼古丁处理大鼠中花生四烯酸诱导的降压反应。在对照动物和尼古丁处理的动物中，PGI2、PGE2和硝普钠诱导的低血压程度相似。提示长期尼古丁处理增强对花生四烯酸的降压反应可能是由于其血管活性代谢产物（即前列环素和/或血栓素A2）的生成和/或清除发生了变化。
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