Fitts D A
Department of Psychology, University of Washington, Seattle 98195.
Pharmacol Biochem Behav. 1993 May;45(1):35-43. doi: 10.1016/0091-3057(93)90082-5.
Reportedly both angiotensin II (ANG II) and angiotensin-converting enzyme (ACE) inhibitors reduce ethanol intake when they are injected SC into certain chronic experimental conditions in the rat. The ACE inhibitors are suggested to reduce ethanol intake by increasing ANG II synthesis in the brain. The present results show that several different methods can produce opposite effects of ANG II and the ACE inhibitor captopril on ethanol intake. Continuous intraventricular infusions of ANG II for 7 days or low doses of oral or SC-infused captopril for up to 12 days increased the intake of ethanol. The only reduction of ethanol intake resulted from a universal blockade of all ACE in both the brain and periphery, a condition in which ANG II could not possibly mediate the decrease. The results contradict the hypothesis that ethanol intake is suppressed by centrally acting or centrally synthesized ANG II. ACE inhibitors may reduce ethanol intake only when they affect the brain as well as the periphery.
据报道，在大鼠的某些慢性实验条件下，当将血管紧张素II（ANG II）和血管紧张素转换酶（ACE）抑制剂皮下注射时，二者均可减少乙醇摄入量。有人认为ACE抑制剂通过增加大脑中ANG II的合成来减少乙醇摄入量。目前的结果表明，几种不同的方法可使ANG II和ACE抑制剂卡托普利对乙醇摄入量产生相反的作用。连续7天脑室内输注ANG II或长达12天口服或皮下注射低剂量卡托普利均可增加乙醇摄入量。唯一使乙醇摄入量减少的情况是大脑和外周所有ACE均被全面阻断，在这种情况下ANG II不可能介导乙醇摄入量的减少。这些结果与以下假设相矛盾，即乙醇摄入量受中枢作用或中枢合成的ANG II抑制。ACE抑制剂可能仅在影响大脑和外周时才会减少乙醇摄入量。
