title: The osmotically and histamine-induced enhancement of the plasma vasopressin level is diminished by intracerebroventricularly administered orexin in rats.
abstract: The effects of the centrally administered neuropeptides orexin-A on water intake and vasopressin (VP) secretion were studied in male Wistar rats (180-250 g). Different doses (10, 30, and 90 μg/10 μl) of the orexins and the specific orexin receptor-1 (OX(1)) antagonist SB 408124 (30 μg/10 μl) were administered intracerebroventricularly (i.c.v.) under anaesthesia, and the water consumption was measured during 6 h. A plasma VP level elevation was induced by histamine (10 mg/kg) or 2.5% NaCl (10 ml/kg) administered intraperitoneally (i.p.). The plasma VP levels were measured by radioimmunoassay. Increased water consumption was observed after the administration of 30 μg/10 μl orexin-A. There were no changes in basal VP secretion after the administration of different doses of the orexins. A significant increase in plasma VP concentration was detected following histamine administration. After 2.5% NaCl administration, there was a moderate VP level enhancement. Intracerebroventricularly administered orexin-A (30 μg/10 μl) blocked the VP level increase induced by either histamine or 2.5% NaCl administration. The inhibitory effects were prevented by the specific OX(1) receptor antagonist. In conclusion, the orexins increased water consumption. After 30 μg/10 μl orexin-A administration, the polydipsia was more pronounced. The OX(1) receptor antagonist significantly decreased the polydipsia. Histamine or hyperosmotic VP release enhancement was blocked by previously administered orexin. This inhibition was not observed following OX(1) receptor antagonist administration. Our results suggest that the effects of the orexins on water consumption or blockade of the histamine and osmosis-induced VP level increase are mediated by the OX(1) receptor.
authors.affiliation: Department of Physiology, Anatomy and Neurosciences, Faculty of Science and Informatics, University of Szeged, Szeged, Közép fasor 52, Hungary.
authors.forename: Gyöngyi K
authors.initials: GK
authors.lastname: Kis
authors.forename: Andor H
authors.initials: AH
authors.lastname: Molnár
authors.forename: Leila
authors.initials: L
authors.lastname: Daruka
authors.forename: János
authors.initials: J
authors.lastname: Gardi
authors.forename: Kinga
authors.initials: K
authors.lastname: Rákosi
authors.forename: Ferenc
authors.initials: F
authors.lastname: László
authors.forename: Ferenc A
authors.initials: FA
authors.lastname: László
authors.forename: Csaba
authors.initials: C
authors.lastname: Varga
mesh_terms: D000818:Animals; D004326:Drinking / Q000187:drug effects / Q000502:physiology; D006632:Histamine / Q000378:metabolism* / Q000494:pharmacology; D007276:Injections, Intraventricular; D047908:Intracellular Signaling Peptides and Proteins / Q000008:administration & dosage*; D008297:Male; D009479:Neuropeptides / Q000008:administration & dosage*; D018377:Neurotransmitter Agents / Q000008:administration & dosage; D064446:Orexin Receptors; D000068797:Orexins; D009997:Osmotic Pressure; D010671:Phenylurea Compounds / Q000494:pharmacology; D059606:Polydipsia / Q000139:chemically induced; D051381:Rats; D017208:Rats, Wistar; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000502:physiology; D018013:Receptors, Neuropeptide / Q000037:antagonists & inhibitors / Q000502:physiology; D014667:Vasopressins / Q000097:blood* / Q000378:metabolism
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D009479:Neuropeptides; D018377:Neurotransmitter Agents; D064446:Orexin Receptors; D000068797:Orexins; D010671:Phenylurea Compounds; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; C542397:SB 408124; D014667:Vasopressins; D006632:Histamine