Plasma angiotensin II concentrations and experimentally induced thirst.
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.
D000804:Angiotensin II / Q000097:blood*; D000818:Animals; D004327:Drinking Behavior / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010953:Plasma Volume; D011092:Polyethylene Glycols / Q000494:pharmacology; D051381:Rats; D013894:Thirst / Q000502:physiology*
D000804:Angiotensin II; D011092:Polyethylene Glycols; D007545:Isoproterenol