Dehydration natriuresis in male rats is mediated by oxytocin

Wan Huang, Siu Lan Lee, Sighvatur S. Arnason, Mats Sjöquist*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

69 Citations (Scopus)


In a previous study in rats we demonstrated the existence of osmoregulatory natriuretic mechanisms distinct from the natriuretic mechanisms that are dependent on volume stimulation. At the same time, we found that oxytocin (OT) receptors were important mediators of natriuresis induced by hypernatremia but not of that induced by isotonic volume expansion. In the present study, the role of OT in dehydration natriuresis was examined in conscious rats. Dehydration for 24 h caused hypernatremia (from 142.1 ± 0.4 to 147.7 ± 0.7 mmol/l) and natriuresis accompanied by an ~30% spontaneous reduction of food intake. In conjunction with renal retention of water caused by an increase in circulating vasopressin, the natriuresis and probably the reduction of food intake can help to counteract the rise in body fluid osmolality. This natriuresis could not be fully explained by the reduction in plasma aldosterone. Plasma OT concentration had increased from 15.5 ± 1.2 to 23.8 ± 2.0 pg/ml at the end of 24 h of dehydration. Intravenous infusion of a selective OT-receptor antagonist [Mpa1,D-Tyr(Et)2,Thr4,Orn8]-OT using osmotic minipumps prevented dehydration natriuresis. It is concluded that in a dehydration-induced hypernatremic state OT is released, inducing natriuresis and facilitating sodium homeostasis. This mechanism is activated by Na osmoreceptors, but is not primarily dependent on the volume status.

Original languageEnglish
Pages (from-to)R427-R433
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number2 39-2
Publication statusPublished - 1996

Other keywords

  • extra-cellular fluid volume regulation
  • oxytocin-receptor antagonist
  • renal sodium excretion
  • sodium balance


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