PMID- 1407380
OWN - NLM
STAT- MEDLINE
DCOM- 19921030
LR  - 20181130
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 56
IP  - 2
DP  - 1992 Aug
TI  - Central oxytocin mediates inhibition of sodium appetite by naloxone in 
      hypovolemic rats.
PG  - 255-63
AB  - Pituitary oxytocin (OT) secretion is inversely related to saline consumption in 
      several experimental models of sodium appetite in rats. Because systemic OT 
      administration does not inhibit sodium appetite, release of OT as a 
      neurotransmitter within the brain, coincident with its secretion from the 
      pituitary, may be related to inhibition of sodium ingestion. The present studies 
      evaluated this possibility by increasing brain OT concentrations both exogenously 
      and endogenously in rats with hypovolemia produced by subcutaneous administration 
      of polyethylene glycol (PEG) solution. Intracerebroventricular (i.c.v.) 
      administration of OT completely abolished intake of 0.5 M NaCl in PEG-treated 
      hypovolemic rats, but did not significantly affect PEG-stimulated water intakes. 
      Endogenous OT secretion was stimulated by systemic treatment with naloxone, which 
      has been shown to increase peripheral and central OT levels. In both one-bottle 
      (0.5 M NaCl) and two-bottle (water and 0.5 M NaCl) drinking tests, 
      intraperitoneal naloxone completely abolished sodium appetite in association with 
      markedly increased pituitary secretion of OT. This inhibition of sodium appetite 
      could be prevented by i.c.v. pretreatment with a specific OT-receptor antagonist, 
      although the antagonist by itself did not affect PEG-stimulated sodium intake. 
      These findings therefore support previous reports which have found that sodium 
      appetite in rats is inhibited by treatments that elicit pituitary release of OT, 
      and provide more direct evidence that brain OT is causally involved in the 
      inhibition of sodium appetite stimulated by such treatments in rats.
FAU - Blackburn, R E
AU  - Blackburn RE
AD  - Department of Behavioral Neuroscience, University of Pittsburgh, Pa 15261.
FAU - Stricker, E M
AU  - Stricker EM
FAU - Verbalis, J G
AU  - Verbalis JG
LA  - eng
GR  - MH25140/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Sodium, Dietary)
RN  - 36B82AMQ7N (Naloxone)
RN  - 3WJQ0SDW1A (Polyethylene Glycols)
RN  - 50-56-6 (Oxytocin)
RN  - 77327-45-8 (oxytocin,1-(beta-mercapto-(beta, beta-cyclopentamethylene)propionic 
      acid)-Tyr(OMe)(2)-Orn(8)-)
SB  - IM
MH  - Animals
MH  - Drinking/drug effects
MH  - Injections, Intraventricular
MH  - Male
MH  - Naloxone/*pharmacology
MH  - Oxytocin/administration & dosage/analogs & derivatives/pharmacology/*physiology
MH  - Plasma Volume/drug effects/*physiology
MH  - Polyethylene Glycols/pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium, Dietary/*administration & dosage
EDAT- 1992/08/01 00:00
MHDA- 1992/08/01 00:01
CRDT- 1992/08/01 00:00
PHST- 1992/08/01 00:00 [pubmed]
PHST- 1992/08/01 00:01 [medline]
PHST- 1992/08/01 00:00 [entrez]
AID - 10.1159/000126236 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1992 Aug;56(2):255-63. doi: 10.1159/000126236.