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AJP - Regulatory, Integrative and Comparative Physiology, Vol 238, Issue 5 372-R377, Copyright © 1980 by American Physiological Society
ARTICLES |
J. F. Mann, A. K. Johnson and D. Ganten
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.
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