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.