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pubmed-article:1581842pubmed:abstractTextPeripheral administration of vasopressin (VP) was previously shown to exert a negative feedback influence on its own release and on the release of oxytocin (OT). In this study we examined the possible influence that OT has on the function of hypothalamic magnocellular neurones. Oxytocin was administered intraperitoneally and its effects on release from VP neurones and from OT neurones were determined as indexed by plasma concentrations of vasopressin-associated neurophysin ([VP-RNP]) and oxytocin-associated neurophysin ([OT-RNP]) under basal conditions and conditions of high plasma osmolality (Posm) induced by acute salt loading. Studies were performed on conscious, chronically instrumented Long-Evans rats. Oxytocin (1 nmol or 10 nmol) dissolved in 1 mL of 0.9% saline was administered intraperitoneally to animals 1 h before they received an intravenous infusion of hypertonic saline over 60 min at a rate designed to raise Posm by approximately 0.75 mosmol.min-1. Intraperitoneal injection of vehicle or 1 nmol of OT did not significantly alter [VP-RNP], [OT-RNP], or basal Posm. Administration of 10 nmol OT also had no effect on [VP-RNP] or [OT-RNP], but this dose of peptide significantly lowered basal Posm (299 +/- 2 to 290 +/- 2 mosmol/kg H2O, p less than 0.001). Both doses of OT did not significantly alter the responsiveness of VP neurones to hyperosmotic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)lld:pubmed
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pubmed-article:1581842pubmed:authorpubmed-author:ChungC WCWlld:pubmed
pubmed-article:1581842pubmed:authorpubmed-author:NorthW GWGlld:pubmed
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pubmed-article:1581842pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:1581842pubmed:articleTitleAbsence of negative feedback by oxytocin on release from magnocellular neurones in conscious rats.lld:pubmed
pubmed-article:1581842pubmed:affiliationDepartment of Physiology, Dartmouth Medical School, Hanover, NH 03756.lld:pubmed
pubmed-article:1581842pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1581842pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed