Cellular dehydration and hypovolemia: effect of acetylsalicylic acid on drinking.
Chronic oral administration of acetylsalicylic acid (ASA), an inhibitor of prostaglandin synthesis, reduces the latency with which rats begin drinking in response to hypovolemia but has no effect on the total amount of water consumed to this stimulus. When drinking is due to cellular dehydration, latency to drink is unaffected while total water intake is markedly augmented by ASA-pretreatment. Chronic, low-dose exposure to ASA or indomethacin has no effect on plasma levels of the dipsogen, angiotensin II. These data, taken in conjunction with previous work demonstrating a suppression of drinking following administration of exogenous prostaglandin E, support the contention that the E prostaglandins are involved in the physiological control of water intake, but suggest that the precise role of the prostaglandin in controlling consumption is dependent upon the stimulus eliciting the behavior.
D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001826:Body Fluids / Q000502:physiology; D003681:Dehydration / Q000523:psychology*; D004327:Drinking Behavior / Q000187:drug effects*; D008297:Male; D011092:Polyethylene Glycols / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats; D013997:Time Factors
D011453:Prostaglandins; D011458:Prostaglandins E; D000804:Angiotensin II; D011092:Polyethylene Glycols; D001241:Aspirin