Rolls B J, Wood R J
Pharmacol Biochem Behav. 1977 Mar;6(3):245-50. doi: 10.1016/0091-3057(77)90020-x.
Angiotensin is a potent dipsogenic substance and causes elevated water intake in some pathological conditions but as yet no physiological role for angiotensin in normal thirst has been proven. If angiotensin is important in normal drinking, then it should contribute to the drinking which follows water deprivation. The rehydration of bilaterally nephrectomized rats, rats with bilateral ureteric ligation and control rats was compared after 21 hours of water deprivation. The total intake during the 6 hour rehydration was the same in the 3 groups despite the differences in the level of circulating angiotensin. Thus the renal renin-angiotensin system is not essential for deprivation-induced drinking. Another way to test any contribution to drinking by angiotensin is the administration of the competitive angiotensin inhibitor, saralasin acetate. In a control experiment saralasin acetate was found to block the dipsogenic effect of intravenous angiotensin. The infusion of saralasin acetate in a wide range of doses did not, however, affect the drinking following ligation of the inferior vena cava. Thus angiotensin is not essential for drinking following caval ligation. Two possible explanations for these results are that angiotensin is not normally involved in these types of thirst or that there is redundancy in the control of drinking with compensation for blocked mechanisms.
血管紧张素是一种有效的致渴物质，在某些病理状态下会导致饮水量增加，但血管紧张素在正常口渴机制中的生理作用尚未得到证实。如果血管紧张素在正常饮水过程中起重要作用，那么它应该会促使动物在禁水后饮水。对双侧肾切除大鼠、双侧输尿管结扎大鼠和对照大鼠在禁水21小时后进行补液情况的比较。尽管循环中的血管紧张素水平存在差异，但三组大鼠在6小时补液期间的总饮水量相同。因此，肾素 - 血管紧张素系统对于禁水诱导的饮水并非必不可少。检测血管紧张素对饮水作用的另一种方法是给予竞争性血管紧张素抑制剂——醋酸沙拉新。在一项对照实验中，发现醋酸沙拉新可阻断静脉注射血管紧张素的致渴作用。然而，输注各种剂量的醋酸沙拉新都不会影响下腔静脉结扎后的饮水情况。因此，血管紧张素对于腔静脉结扎后的饮水并非必不可少。对这些结果有两种可能的解释：一是血管紧张素通常不参与这类口渴机制；二是在饮水控制方面存在冗余机制，能够补偿被阻断的机制。
