Dehydration natriuresis in male rats is mediated by oxytocin .
Huang, Wan, Siu-Lan Lee, Sighvatur S. Arnason, and Mats
Sj[diaeresis]oquist.
Department of Physiology and Medical Biophysics, Biomedical Center,
Uppsala University, Uppsala, Sweden
APStracts 2:0275R, 1995.
In a previous study in rats we demonstrated the existence of
osmoregulatory natriuretic mechanisms as 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 a 30% voluntary
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 hours 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.
Received 4 April 1995; accepted in final form 1 September 1995.
APS Manuscript Number R225-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 November 95