RENAL NERVE TRANSECTION INHIBITS DRINKING ELICITED BY EATING AND BY INTRAGASTRIC OSMOTIC LOADS IN RATS

Adult Sprague-Dawley male rats surgically equipped with a chronic gast ric catheter were tested for drinking after 2 ml intragastric infusion s of 290, 600, 900, 1200, or 1800 mOsm/kg NaCl. Rats with bilateral tr ansection of renal nerves (RD) drank less than neurologically intact r ats (S) after 600 and 900 mOsm/kg NaCl infusions. The RD rats were cap able of a rapid and robust drinking response to relatively mild experi mental challenges, because they drank appropriately in response to SC angiotensin II and to a dose of histamine that is a threshold dose for increasing water intake. The RD rats ate less than S rats, but RD rat s drank appropriate amounts of water when eating and drinking after 24 -h food deprivation. When nondeprived and ingesting one, two, or four small (0.57 g) salted crackers, the RD rats drank significantly less w ater than S rats. At the time drinking was initiated after ingestion o f one salted cracker, plasma osmolality, sodium, protein, and packed c ell volume were not changed from baseline conditions (i.e., no eating) in neurologically intact rats; plasma renin activity was significantl y elevated at the time drinking was initiated following the ingestion of one or two small crackers. These findings (a) demonstrate a role fo r renal nerves in drinking behavior in rats, and (b) suggest the worki ng hypothesis that the ingestion of a small meal, and the subsequent d elivery of a relatively small osmotic load to the gastrointestinal tra ct and/or hepatic-portal vein, activates mechanisms for drinking that include a change in activity of renal nerves to increase plasma renin activity without cellular dehydration or hypovolemia. Such mechanisms may be activated to mobilize drinking behavior in advance of postprand ial fluid deficit.