Endocrine consequences of prenatal sodium depletion prepare rats for high need-free NaCl intake in adulthood.

Offspring of dams that were repeatedly sodium depleted during late pregnancy (at days 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 depletion 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 nonneonatally sodium depleted. Trunk blood taken from dams at day E18, i.e., 24 h after the second treatment, revealed that sodium depletion produced marked increases in the dam's plasma angiotensin (ANG) II and aldosterone that were not present when dams were treated with captopril during sodium depletion, even though both groups displayed a similar hyponatremia. We therefore propose that, during prenatal sodium depletion, the activation of the angiotensin-aldosterone system rather than the loss of sodium itself is responsible for the modification in need-free NaCl intake behavior. Finally, we suggest that, during pregnancy, ANG II may have an organizational effect on the neural substrate in the fetal brain that subserves subsequent NaCl intake behavior.