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 gastric catheter were tested for drinking after 2 ml intragastric infusions of 290, 600, 900, 1200, or 1800 mOsm/kg Nacl. Rats with bilateral transection of renal nerves (RD) drank less than neurologically intact rats (S) after 600 and 900 mOsm/kg NaCl infusions. The RD rats were capable of a rapid and robust drinking response to relatively mild experimental challenges, because they drank appropriately in response to s.c. angiotensin II and to dose of histamine that is a threshold dose for increasing water intake. The RD rats ate less than S rats, but RD rats 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 water than S rats. At the time drinking was initiated after ingestion of one salted cracker, plasma osmolality, sodium, protein, and packed cell volume were not changed from baseline conditions (i.e., no eating) in neurologically intact rats; plasma renin activity was significantly elevated at the time drinking was initiated following the ingestion of one or two small crackers. These findings (a) demonstrate a role for renal nerves in drinking behavior in rats, and (b) suggest the working hypothesis that the ingestion of a small meal, and the subsequent delivery of a relatively small osmotic load to the gastrointestinal tract 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 postprandial fluid deficit.