Pohorecky L A
Alcohol. 1986 Sep-Oct;3(5):283-6. doi: 10.1016/0741-8329(86)90002-9.
Previous research from this laboratory indicated that noradrenergic mechanisms mediate ethanol diuresis. Experiments described here examined changes in sensitivity of these noradrenergic mechanisms in animals chronically treated with ethanol. Norepinephrine hydrochloride (0-12 micrograms intraventricularly) produced dose-dependent diuresis in control (dextrin maltose)- and ethanol (8-11 g/kg/day)-treated rats on the first day of treatment. Tolerance to ethanol diuresis was present after 10 days of ethanol treatment. Lack of responsiveness to norepinephrine-induced diuresis was evident only on the 20th day of treatment in both ethanol and dextrin-maltose groups of rats. These results suggest that norepinephrine does not play a primary role in the development of tolerance to the diuretic action of ethanol.
该实验室先前的研究表明,去甲肾上腺素能机制介导乙醇利尿作用。此处描述的实验研究了长期用乙醇处理的动物中这些去甲肾上腺素能机制的敏感性变化。在处理的第一天,盐酸去甲肾上腺素(脑室内注射0 - 12微克)在对照(糊精麦芽糖)处理和乙醇(8 - 11克/千克/天)处理的大鼠中产生剂量依赖性利尿作用。乙醇处理10天后出现对乙醇利尿作用的耐受性。在处理的第20天,乙醇组和糊精麦芽糖组大鼠对去甲肾上腺素诱导的利尿作用均明显缺乏反应。这些结果表明,去甲肾上腺素在对乙醇利尿作用的耐受性发展中不发挥主要作用。