Johnson A K, Mann J F, Rascher W, Johnson J K, Ganten D
Am J Physiol. 1981 Mar;240(3):R229-34. doi: 10.1152/ajpregu.1981.240.3.R229.
The systemic administration of angiotensin II or its precursors will result in increased water intake. Several manipulations that result in hypovolemia and/or hypotension (extracellular thirst challenges) are known to activate the peripheral renin-angiotensin system and also produce drinking. Although there are without question multiple mediators of thirst associated with extracellular thirst challenges, one of the major factors responsible for water intake has been hypothesized to be the action of angiotensin II. In the experimental analysis of thirst, several types of hypovolemic-hypotensive manipulations have been employed. However, there is a paucity of data available that characterize the systematic changes of angiotensin II levels following such challenges. The present studies determined plasma angiotensin II levels and drinking responses after isoproterenol administration, caval ligation, and subcutaneous polyethylene glycol treatment. The experimental protocols for treatment of the animals closely approximated conditions commonly employed in the experimental analysis of thirst. The results indicated that endogenous levels of angiotensin II increase after these treatments to levels that in all likelihood are sufficient to make a substantial contribution to the drinking response.
血管紧张素II或其前体的全身给药会导致饮水量增加。已知几种导致血容量减少和/或低血压的操作（细胞外渴觉刺激）会激活外周肾素-血管紧张素系统并引发饮水行为。尽管毫无疑问，与细胞外渴觉刺激相关的渴觉有多种介质，但据推测，导致饮水的主要因素之一是血管紧张素II的作用。在渴觉的实验分析中，已采用了几种类型的血容量减少性低血压操作。然而，关于此类刺激后血管紧张素II水平的系统性变化，现有数据很少。本研究测定了给予异丙肾上腺素、腔静脉结扎和皮下注射聚乙二醇后血浆血管紧张素II水平和饮水反应。治疗动物的实验方案与渴觉实验分析中常用的条件非常接近。结果表明，这些治疗后血管紧张素II的内源性水平会升高到很可能足以对饮水反应做出重大贡献的水平。
