Dehydration natriuresis in male rats is mediated by oxytocin

Abstract

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 approximately 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.

Renal and Hormonal Effects of Water Deprivation in Late-Term Pregnant Rats

“…19 WD caused a significant reduction in plasma volume and a rise in hematocrit, which is concordant with previous results. 20 We had expected that because pregnant rats were actively retaining water, WD could cause a greater reduction on plasma volume in this group. However, the percentage decrease in plasma volume was almost identical to that observed in nonpregnant rats.…”

Contribution of endogenous oxytocin to sodium excretion in anaesthetized, surgically operated rats

“…Oxytocin release is known to be stimulated by dehydration (Windle et al 1993, Huang et al 1996, hypertonic saline loading (Balment et al 1980, Huang et al 1995 and partial nephrectomy (Huang et al 1994), i.e. situations which all result in enhanced sodium excretion (in the latter case by the surviving nephrons).…”

“…However, only fragmentary information is available concerning the effects of oxytocin antagonists in the absence of infused hormone. Huang et al (1996) administered an antagonist by osmotic minipump to conscious rats and observed a small reduction in sodium excretion, but the significance of this was obscured by a comparable reduction in sodium intake (as a result of the minipump implantation procedure). Similarly, a study in anaesthetized animals showed a small (non-significant) reduction in sodium excretion, but the antagonist was administered for only 60 min before a confounding manoeuvre (unilateral nephrectomy) was superimposed (Huang et al 1994).…”

Osmoregulation Requires Brain Expression of the Renal Na-K-2Cl Cotransporter NKCC2

“…The HNS also produces the closely related hormone oxytocin (OXT), which acts to promote kidney natriuresis (Huang et al, 1996). Single-cell RT-PCR enables AVP and OXT transcripts to be detected in the same MCN (Glasgow et al, 1999), but the expression levels of each neuropeptide RNA differ by orders of magnitude.…”