Water and salt intake of wild @entity95 ( XXXX (L)) following dipsogenic stimuli.

@entity2656 @entity548 @entity1219 @entity3791 @entity8723 @entity95 @entity1372 @entity413 @entity3282 @entity4338
Wild @entity95 trapped in their natural habitat and adapted to laboratory conditions were studied. Food, water and electrolyte (0.5 M- @entity1219 , 0.5 M- @entity4338 , 0.25 M- @entity8723 and 0.25 M- @entity3282 ) consumption, urinary volume and @entity1372 losses were monitored daily following stimuli which were found dipsogenic in other species. Water drinking was observed immediately after the intravenous injection of 1 M- @entity1219 (3 ml/kg), and following withdrawal of a mean of 13.9% of calculated blood volume. Daily intake of water decreased during intracerebroventricular (I.C.V.) infusion of 0.3 M- @entity1219 in artificial cerebrospinal fluid (c.s.f.), during I.C.V. infusion of 0.9 M- @entity2656 c.s.f., both at a rate of 17 microliters/h, following peritoneal dialysis with 5% (w/v) @entity413 solution, and during food restriction. Water intake was not affected following intravenous administration of @entity3791 (10 mg/kg). Daily intake of 0.5 M- @entity1219 solution was increased following peritoneal dialysis with 5% (w/v) @entity413 solution, which caused hyponatraemia, but not after @entity548 which caused about the same @entity1372 deficit as peritoneal dialysis, but as an isosmotic loss. Administration of two different angiotensin II analogues, systemically or I.C.V., failed to induce water drinking. However, urinary @entity1372 excretion and intake of 0.5 M- @entity1219 were increased during the 5 days of I.C.V. infusion of angiotensin II (10 pmol/h). Infusion for 1 day of angiotensin II (500 pmol/h) led to increased urinary @entity1372 excretion which was followed by increased intake. The intake of other electrolyte solutions was not significantly affected by any of the treatments detailed above. The mechanisms participating in initiation of thirst in wild @entity95 are very sensitive to decrease in blood volume, in contrast to other species studied in laboratories. Angiotensin II at the doses and routes administered was not dipsogenic in wild @entity95 . The increased intake of 0.5 M- @entity1219 solution observed during and after the long-term intraventricular administration of angiotensin II in the wild @entity95 appears predominantly a response to @entity1372 deficit caused by natriuresis. The persistence of appetite after the cessation of infusion is indicative of a residual effect on central mechanisms of salt appetite.
