Development of the drinking deficit to hypertonic saline in rats after abdominal vagotomy.
After abdominal vagotomy, rats drink significantly less water in response to hypertonic saline. The drinking deficit could be due to the disconnection of vagal afferent fibers from a peripheral receptor stimulated by hypertonic saline or the loss of a more complex, tonic, fascilitatory function. The loss of the phasic afferent fiber function should appear immediately after vagotomy, but the loss of the tonic function might take more time to develop. We attempted to distinguish between these two possibilities by preparing 5 different groups of vagotomized rats that were each tested with 1 M NaCl (1% BW) at one of five postoperative days--2, 4, 7, 14 or 21 days. The drinking response was significantly decreased from preoperative intake in the groups tested on postoperative days 7, 14, and 21, but not in the groups tested on postoperative days 2 and 4. Since the drinking deficit is not present 2 and 4 days after vagotomy, the effect of vagotomy is not the result of lesioning afferent fibers that mediate a peripheral phasic stimulation elicited by hypertonic saline. The postoperative delay of at least 7 days for the deficit to appear suggests that the effect of vagotomy is the loss of some more complex neurological function that is necessary for a normal drinking response. The nature of this lost function is unknown.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D004327:Drinking Behavior / Q000187:drug effects / Q000502:physiology*; D006982:Hypertonic Solutions; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D011930:Reaction Time / Q000502:physiology; D012965:Sodium Chloride / Q000494:pharmacology*; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology*
D006982:Hypertonic Solutions; D000804:Angiotensin II; D012965:Sodium Chloride