Thirst impairment elicited by intraventricular administration of vasopressin antagonists.

To determine whether centrally released vasopressin influences thirst, observations of osmotic thirst threshold, osmotic load excretion and postloading restitution of plasma osmolality were made in dogs in control experiments and during infusion of AVP antagonists into the third ventricle. Significant elevation of osmotic thirst threshold was elicited by infusion of d(CH2)5AVP at a rate of 0.2-2.0 micrograms.min-1 and of d(Et2)AVP at a rate of 0.3 micrograms.min-1 (V1 antagonists, weak V2 agonists) as well as by administration of d(CH2)5[D-Ile2,Abu4]AVP at a rate of 0.4 micrograms.min-1 (potent V2 antagonist, weak V1 antagonist). Administration of d(CH2)5AVP at a rate of 2.0 micrograms.min-1 was associated with a significant suppression of the postloading water intake and osmotic load excretion and with a delay in restitution of plasma osmolality. These findings indicate that centrally released vasopressin may participate in the control of thirst.