Exogenous central angiotensin fails to stimulate a sodium appetite in diabetes insipidus Brattleboro rats.

We investigated the effect of central administration of angiotensin II (AngII) on a specific salt appetite (SSA) in homozygous diabetes insipidus Brattleboro (DI) rats because this stimulus induces such a response in all other rat strains. DI rats have a deficiency in the synthesis of arginine vasopressin (AVP) and a reduced content of pituitary oxytocin (OT). They are characterized also by polyuria, polydipsia, and they seldom ingest high concentrations of NaCl solutions. We also tested if the appetite can be influenced by neurohypophyseal hormones especially oxytocin (OT) because it inhibits SSA in other animals. DI rats and Long Evans (LE) controls were fed ad libitum and given a choice between water, and either 0.9% or 1.8% NaCl. The data showed a significant increase of daily spontaneous water intake in DI compared with LE rats. Both DI and LE ingested similar small spontaneous volumes of the isotonic NaCl solution, but DI rats drank significantly less hypertonic NaCl than the LE controls. I.c.v infusion of AngII induced significant sodium intake in LE rats, but only raised water intake in DI rats. When combined with i.c.v. Ang II, OVT enhanced salt intake in LE animals while AVP attenuated water intake in both groups of rats and blocked NaCl intake completely in LE rats. In conclusion, DI rats did not demonstrate a SSA in response to central administration of AngII, although the drinking of water was enhanced. In combination with i.c.v. AngII, AVP inhibits water drinking in both DI and LE rats. In the LE controls OT attenuates AngII-induced SSA but has no effect in DI rats.