The endocrine consequences of prenatal sodium depletion prepare rats for high need-free nacl intake in adulthood. Galaverna, O., S. Nicolaidis, S-Z. Yao, R. R. Sakai, and A. N. Epstein. University of Pennsylvania, Dept. of Biology, Philadelphia PA 19104, and College de France, Paris France.
APStracts 2:0053R, 1995.
Offspring of dams that were repeatedly sodium depleted during late pregnancy (at E14, E17 and E20) expressed high need-free 3% NaCl intake in adulthood. Need-free 3% NaCl intake was greater in females, thereby respecting the sexual dimorphism of this behavior, and was increased further by successive sodium depletions in adulthood. Offspring from dams that had been sodium depleted while receiving the angiotensin-converting enzyme inhibitor Captopril showed a need-free NaCl intake similar to that of control rats non-neonatally sodium depleted. Trunk blood taken from dams at E18, i.e., 24 hours after the second treatment, revealed that sodium depletion produced marked increases in the dam's plasma angiotensin II and aldosterone that were not present when dams were treated with Captopril during sodium depletion even though both groups displayed a similar hyponatremia. Therefore we propose that during the prenatal sodium depletion it is the activation of the angiotensin-aldosterone system rather than the loss of sodium itself that is responsible for the modification in need-free NaCl intake behavior. Finally, we suggest that, during pregnancy, angiotensin II may have an organizational effect on the neural substrate in the fetal brain that subserves subsequent NaCl intake behavior. 

Received 6 January 1993; accepted in final form 21 February 1995.
APS Manuscript Number R005-3.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  7 March 1995.