Thirst impairment elicited by intraventricular administration of vasopressin antagonists

• Published in: Peptides (New York, N.Y. : 1980) Vol. 8; no. 6; pp. 1003 - 1009
• Main Authors: Szczepanska-Sadowska, Ewa, Sobocinska, Jadwiga, KozŁowski, StanisŁaw
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.11.1987; Elsevier Science
• Subjects: Animals; Arginine Vasopressin - administration & dosage; Arginine Vasopressin - analogs & derivatives; Arginine Vasopressin - pharmacology; AVP antagonists; Biological and medical sciences; Body Temperature - drug effects; Dogs; Eating - drug effects; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Injections, Intraventricular; Male; Osmolar Concentration; Osmoregulation; Receptors, Angiotensin - drug effects; Receptors, Angiotensin - physiology; Receptors, Vasopressin; Thirst; Thirst - drug effects; Vasopressin; Vasopressins - antagonists & inhibitors; Vasopressins - physiology; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Osmoregulation; AVP antagonists; Thirst; Vasopressin; Fissipedia; Carnivora; Feeding behavior; Peptide hormone; Neuropeptide; Vertebrata; Mammalia; Hormonal regulation; Intracerebral administration; Beverage; Dog
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/0196-9781(87)90128-8

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(CH 2) 5AVP at a rate of 0.2–2.0 μg·min −1 and of d(Et 2)AVP at a rate of 0.3 μg·min −1 (V 1 antagonists, weak V 2 agonists) as well as by administration of d(CH 2) 5[D-Ile 2,Abu 4]AVP at a rate of 0.4 μg·min −1 (potent V 2 antagonist, weak V 1 antagonist). Administration of d(CH 2) 5AVP at a rate of 2.0 μg·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.