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J Appl Physiol 87: 1440-1447, 1999;
8750-7587/99 $5.00
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Vol. 87, Issue 4, 1440-1447, October 1999

INVITED REVIEW
Fetal diuretic responses to maternal hyponatremia: contribution of placental sodium gradient

Todd J. Roberts, Mark J. M. Nijland, Leslee Williams, and Michael G. Ross

Perinatal Research Laboratories, Department of Obstetrics and Gynecology, University of California Los Angeles School of Medicine, Harbor-UCLA Medical Center, Torrance, California 90502

Maternal hyponatremia induces fetal hyponatremia and increased fetal urine flow. We sought to examine the relative contributions of the placental Na+ gradient vs. the absolute decrease in fetal plasma Na+ in the fetal diuretic response to hyponatremia. Seven ewes with singleton fetuses (130 ± 2 days) were prepared. Ewes received intravenous 1-desamino-8-D-arginine vasopressin (20 µg) and warm tap water (2 liters). Maternal plasma Na+ was decreased to achieve two levels of maternal hyponatremia. Maternal and fetal blood volume were measured with radiolabeled red blood cells. In response to the first decrease in maternal plasma Na+, fetal plasma Na+ did not change initially. Subsequently, fetal plasma Na+ decreased, normalizing the gradient. The second decrease in maternal plasma Na+ similarly induced a reduced and normalized placental gradient at lower fetal plasma Na+ values. Fetal urine flow increased in direct proportion to the degree of fetal hyponatremia (13, 38, 63, 100%, respectively). Maternal, although not fetal, blood volume significantly increased in response to hyponatremia. These results suggest that chronic fetal hyponatremia will result in a persistent diuresis, despite placental equilibration.

pregnancy; amniotic fluid; fetal sheep; 1-desamino-8-D-arginine vasopressin; hyposmolality


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[Abstract] [Full Text] [PDF]




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