Plasma angiotensin II concentrations and experimentally induced thirst

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Abstract
The systemic administration of angiotensin [A] II or its precursors will result in increased H2O intake. Several manipulations that result in hypovolemia and/or hypotension (extracellular thirst challenges) are known to activate the peripheral renin-A system and also produce drinking. Although there definitely are multiple mediators of thirst associated with extracellular thirst challenges, one of the major factors responsible for H2O intake has been hypothesized to be the action of AII. In the experimental analysis of thirst, several types of hypovolemic-hypotensive manipulations were employed. Plasma AII levels and drinking responses were determined after isoproterenol administration, caval ligation, and s.c. polyethylene glycol treatment. The experimental protocols for treatment of the rats closely approximated conditions commonly employed in the experimental analysis of thirst. The results indicated that endogenous levels of AII increase after these treatments to levels that in all likelihood are sufficient to make a substantial contribution to the drinking response.

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