DEHYDRATION NATRIURESIS IN MALE-RATS IS MEDIATED BY OXYTOCIN

In a previous study in rats we demonstrated the existence of osmoregul atory natriuretic mechanisms distinct from the natriuretic mechanisms that are dependent on volume stimulation. At the same time, we found t hat oxytocin (OT) receptors were important mediators of natriuresis in duced by hypernatremia but not of that induced by isotonic volume expa nsion. In the present study, the role of OT in dehydration natriuresis was examined in conscious rats. Dehydration for 24 h caused hypernatr emia (from 142.1 +/- 0.4 to 147.7 +/- 0.7 mmol/l) and natriuresis acco mpanied by an similar to 30% spontaneous reduction of food intake. In conjunction with renal retention of water caused by an increase in cir culating vasopressin, the natriuresis and probably the reduction of fo od intake can help to counteract the rise in body fluid osmolality. Th is 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 i nfusion of a selective OT-receptor antagonist [Mpa(1),D-Tyr(Et)(2),Thr (4),Orn(8)]-OT using osmotic minipumps prevented dehydration natriures is. It is concluded that in a dehydration-induced hypernatremic state OT is released, inducing natriuresis and facilitating sodium homeostas is. This mechanism is activated by Na osmoreceptors, but is not primar ily dependent on the volume status.