Plasma angiotensin II: dipsogenic levels and angiotensin-generating capacity of renin

Abstract

Activation of the renin-angiotensin system (RAS) or administration of angiotensin II (AII) will induce H2O intake. In the rat, the species in which the physiological mechanisms of thirst were most thoroughly studied, the circulating AII levels produced by systemic administration of dipsogenic doses of the octapeptide were not established. The capacity of the endogenous RAS to generate AII sufficient to contribute to the production of a thirst state was not well studied. 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 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.