Fetal diuretic responses to maternal hyponatremia: contribution of
placental sodium gradient.
Roberts, Todd J., Mark J. M. Nijland, Leslee Williams, Michael G.
Ross.
1Perinatal Research Laboratories, Department of Obstetrics and
Gynecology, University of California Los Angeles School of Medicine,
Harbor-UCLA Medical Center, 1124 W Carson Street, Torrance, CA 90502
and 2Current address: Department of Veterinary Physiology, Cornell
University, Ithaca, NY 14853.
APStracts 6:0276A, 1999.
Maternal hyponatremia induces fetal hyponatremia and increased fetal
urine flow. In response to acute reductions in maternal plasma sodium
(Na), fetal plasma Na decreases more slowly, altering the placental
Na gradient, until fetal plasma Na equilibrates with maternal values.
We sought to examine the relative contributions of the placental Na
gradient versus the absolute decrease in fetal plasma Na in the fetal
diuretic response to hyponatremia. We hypothesized that the
normalization of the placental gradient would reduce fetal diuretic
responses to chronic maternal hyponatremia. Methods: Seven ewes with
singleton fetuses (130 [angstrom]a 2 d) were prepared with maternal
and fetal vascular catheters, and fetal bladder and amniotic fluid
catheters. After 6 days of recovery, ewes received intravenous DDAVP
(20 *g) and warm tap water (2 _) via a naso-ruminal tube, followed by
a DDAVP infusion (4 *g/h). Maternal plasma Na was decreased to
achieve two levels of maternal hyponatremia (5-7 and 12-15 mEq/l
below control). At each level, fetal urine flow was measured
initially when the gradient was reduced and secondly upon fetal
-maternal Na equilibration. Maternal and fetal blood volume were
measured with radiolabeled red cells. Results: In response to the
first decrease in maternal plasma Na, fetal plasma Na did not change
initially, reducing the placental gradient (6.3 to 2.8 mEq/l).
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 (0.08 [angstrom]a 0.01 ml/kg/min) increased
in direct proportion to the degree of fetal hyponatremia (13, 38, 63,
100%, respectively) with no correlation to the placental gradient.
Maternal, though not fetal blood volume significantly increased in
response to hyponatremia. Conclusions: (1) Maternal hyponatremia
induces fetal urinary diuresis, directly proportionate to the degree
of fetal hyponatremia. (2) The fetal diuretic response is secondary,
in part, to increased GFR and intrarenal mechanisms, and (3) These
results suggest that chronic fetal hyponatremia will result in a
persistent diuresis, despite placental equilibration.
Received 3 September 1998; accepted in final form 4 June 1999.
APS Manuscript Number A792-8.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1999 The American Physiological Society.
Published in APStracts on 25 June 1999