Abstract:
: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.
journal_name
Neuroendocrinologyjournal_title
Neuroendocrinologyauthors
Blackburn RE,Stricker EM,Verbalis JGdoi
10.1159/000126236subject
Has Abstractpub_date
1992-08-01 00:00:00pages
255-63issue
2eissn
0028-3835issn
1423-0194journal_volume
56pub_type
杂志文章abstract::Although previously considered rare, recent epidemiological studies have revealed that the incidence (3.6/100,000) and prevalence (35/100,000) of gastroenteropancreatic neuroendocrine tumors (GEP-NETs) has increased over the past few decades. Despite the progress in the understanding of GEP-NET molecular biology, ther...
journal_title:Neuroendocrinology
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doi:10.1159/000125138
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journal_title:Neuroendocrinology
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doi:10.1159/000124886
更新日期:1988-01-01 00:00:00
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journal_title:Neuroendocrinology
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journal_title:Neuroendocrinology
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更新日期:1984-04-01 00:00:00
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更新日期:1975-01-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
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更新日期:1988-03-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
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journal_title:Neuroendocrinology
pub_type: 杂志文章
doi:10.1159/000124039
更新日期:1984-12-01 00:00:00
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journal_title:Neuroendocrinology
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journal_title:Neuroendocrinology
pub_type: 杂志文章
doi:10.1159/000126399
更新日期:1993-03-01 00:00:00
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doi:10.1159/000054405
更新日期:1999-02-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
doi:10.1159/000122349
更新日期:1975-01-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
doi:10.1159/000126605
更新日期:1993-12-01 00:00:00
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更新日期:1979-01-01 00:00:00
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pub_type: 杂志文章
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更新日期:1995-11-01 00:00:00
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journal_title:Neuroendocrinology
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更新日期:1995-12-01 00:00:00
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journal_title:Neuroendocrinology
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更新日期:1995-01-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
doi:10.1159/000124439
更新日期:1986-01-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
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更新日期:1977-01-01 00:00:00
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更新日期:1992-04-01 00:00:00
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journal_title:Neuroendocrinology
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更新日期:1988-12-01 00:00:00
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更新日期:2003-01-01 00:00:00