Potent stimuli for vasopressin release, hypertonic saline and hemorrhage, cause antipyresis in the rat.
Two potent stimuli for AVP release into the blood, hemorrhage and hypertonic saline, were evaluated for their antipyretic effects in the rat. Hemorrhage of 20% of estimated blood volume reduced brain temperature of febrile but not afebrile rats confirming earlier research in the sheep. Hypertonic saline was also antipyretic in the rat. Hypertonic urea was somewhat less antipyretic whereas hypertonic glucose had no effect on febrile temperatures. AVP release into the peripheral circulation showed the relationship saline greater than urea greater than glucose and parallelled the antipyretic effectiveness of these solutes. The antipyresis caused by hypertonic saline was not significantly different in rats passively immunized intravenously with AVP antiserum than in rats which received hypertonic saline alone. These results provide indirect evidence that endogenous AVP is released in the brain following hemorrhage or hypertonic challenge and that this endogenous AVP can affect central febrile pathways.
D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood / Q000378:metabolism*; D001831:Body Temperature; D001921:Brain / Q000503:physiopathology; D005334:Fever / Q000503:physiopathology*; D006470:Hemorrhage / Q000503:physiopathology*; D008297:Male; D051381:Rats; D012462:Saline Solution, Hypertonic; D012965:Sodium Chloride
D012462:Saline Solution, Hypertonic; D001127:Arginine Vasopressin; D012965:Sodium Chloride