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Oxytocin antisense reduces salt intake in the baroreceptor-denervated rat

M Morris1, P Li, C Barrett

  • 1Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157, USA.

Regulatory Peptides
|October 20, 1995
PubMed

Insights

Central oxytocin (OT) plays a key role in regulating salt intake. Inhibiting OT in denervated rats significantly reduced their sodium chloride consumption, highlighting the oxytocinergic axis

Area of Science:

  • Neuroendocrinology
  • Behavioral Neuroscience
  • Physiology

Background:

  • Central oxytocin (OT) is implicated in regulating fluid and electrolyte balance.
  • Sinoartic denervation (SAD) is known to alter salt appetite.
  • The specific role of central OT in SAD-induced changes in salt intake remains unclear.

Purpose of the Study:

  • To investigate the involvement of central oxytocin in the inhibition of salt intake following sinoartic denervation (SAD).
  • To determine the effect of oxytocin antisense treatment on sodium chloride intake in SAD and sham-operated (SO) rats.

Main Methods:

  • Rats underwent either sinoartic denervation (SAD) or sham operation (SO).
  • Oxytocin (OT) antisense oligodeoxynucleotides (ODNs) or control ODNs were injected into the paraventricular nucleus (PVN).
  • 24-hour intake of 2% NaCl was measured, and plasma OT levels were assessed after salt loading.

Main Results:

  • PVN injection of OT antisense ODNs significantly decreased 2% NaCl intake in SAD rats (8 +/- 4 ml) compared to control ODN-injected SAD rats (22 +/- 4 ml).
  • OT antisense treatment had no effect on salt intake in SO rats.
  • SAD rats exhibited an elevated plasma OT response to salt loading (3.2 +/- 0.7 to 6.9 +/- 0.8 pg/ml), which was not observed in SO rats.

Conclusions:

  • Central oxytocin antisense specifically inhibits salt intake in denervated rats, suggesting a role for the central oxytocinergic system in stimulating sodium drive.
  • The findings indicate that the central oxytocinergic axis is activated by salt loading in SAD rats, contributing to altered salt appetite.

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