Mann J F, Johnson A K, Ganten D
Am J Physiol. 1980 May;238(5):R372-7. doi: 10.1152/ajpregu.1980.238.5.R372.
Activation of the renin-angiotensin system (RAS) or administration of angiotensin II (AII) will induce water intake. In the rat, the species in which the physiological mechanisms of thirst have been most thoroughly studied, the levels of circulating AII produced by systemic administration of dipsogenic doses of the octapeptide have not been established. Furthermore, the capacity of the endogenous RAS to generate AII sufficient to contribute to the production of a thirst state has not been well studied. In the present series of investigations, plasma levels of AII were determined following infusions of the peptide over a range of doses frequently employed in studies on thirst. In addition, a series of manipulations ranging from mild water deprivation or ingestion of a dry meal to ether stress of rats with malignant renal hypertension was applied to examine the capacity of the RAS to generate angiotensin. The results indicate that the endogenous RAS can readily produce the major effector peptide of the system so that circulating levels are well in excess of the dipsogenic threshold for AII.
肾素-血管紧张素系统（RAS）的激活或给予血管紧张素II（AII）会引发饮水行为。在大鼠（对口渴生理机制研究最为透彻的物种）中，通过给予致渴剂量的八肽进行全身给药所产生的循环AII水平尚未确定。此外，内源性RAS产生足以导致口渴状态的AII的能力也未得到充分研究。在本系列研究中，在给予常用于口渴研究的一系列剂量的该肽后，测定了AII的血浆水平。此外，还进行了一系列操作，从轻度缺水或摄入干餐到对恶性肾性高血压大鼠施加乙醚应激，以检查RAS产生血管紧张素的能力。结果表明，内源性RAS能够轻易产生该系统的主要效应肽，从而使循环水平远超过AII的致渴阈值。
