Grupp L A, Killian M, Perlanski E, Stewart R B
Department of Pharmacology, University of Toronto, Ontario, Canada.
Pharmacol Biochem Behav. 1988 Mar;29(3):479-82. doi: 10.1016/0091-3057(88)90007-x.
The voluntary intake of alcohol has been shown to be attenuated by a variety of manipulations which increase activity in the renin-angiotensin system. In the present study we examined the effects of peripheral injections of the peptide angiotensin II on alcohol drinking. The peptide produced a dose-dependent decrease in alcohol intake with 20 micrograms/kg having little effect, 200 micrograms/kg reducing intake by approximately 50% and 1 mg/kg virtually abolishing all alcohol drinking. This decrease was not due to a peptide induced motor deficit, or state of sickness, and could also not be accounted for by the increased water intake, or by a change in pharmacokinetics and taste function. These data provide direct evidence that angiotensin II can modulate voluntary alcohol drinking. The possibility that the level of angiotensin II serves as a satiety signal in alcohol drinking is discussed.
已表明，通过各种增加肾素 - 血管紧张素系统活性的操作，酒精的自愿摄入量会减少。在本研究中，我们检测了外周注射肽类血管紧张素II对酒精饮用的影响。该肽产生了剂量依赖性的酒精摄入量减少，20微克/千克几乎没有效果，200微克/千克使摄入量减少约50%，1毫克/千克几乎消除了所有酒精饮用。这种减少不是由于肽诱导的运动缺陷或疾病状态，也不能通过增加的水摄入量、药代动力学变化或味觉功能改变来解释。这些数据提供了直接证据，表明血管紧张素II可以调节自愿酒精饮用。文中还讨论了血管紧张素II水平在酒精饮用中作为饱腹感信号的可能性。
