A novel model of polyhydramnios: amniotic fluid volume is increased in aquaporin 1 knockout mice.

Abstract:

OBJECTIVE:To test the hypothesis that amniotic fluid volume is increased in aquaporin 1 knockout mice. STUDY DESIGN:Transgenic mice deficient in aquaporin 1 protein were generated by targeted gene disruption, as described previously. After a cesarean section was performed, intact, individual gestational sacs were removed from the uterus and weighed. Amniotic fluid volume, osmolality, and fetal and placental weights were determined. Data were analyzed by a 1-way analysis of variance for ranks; Dunn's post hoc test was used to analyze significant trends. RESULTS:Analysis of 16 litters showed 35 wild-type, 52 heterozygote, and 33 aquaporin 1 knockout mice. The knockout mice had a greater volume of amniotic fluid and lower amniotic fluid osmolality than their wild-type and heterozygote counterparts. There were no significant differences in fetal or placental weights among the groups. CONCLUSIONS:Aquaporin 1 null fetuses produce a greater volume of more dilute amniotic fluid. Our findings show that aquaporin 1 water channels in fetal membranes may contribute to amniotic fluid volume regulation. We speculate that idiopathic polyhydramnios may be associated with a deficiency of aquaporin 1 channels in human fetal membranes. Transgenic aquaporin 1 knockout mice provide a unique animal of polyhydramnios.

journal_name

Am J Obstet Gynecol

authors

Mann SE,Ricke EA,Torres EA,Taylor RN

doi

10.1016/j.ajog.2005.02.046

subject

Has Abstract

pub_date

2005-06-01 00:00:00

pages

2041-4; discussion 2044-6

issue

6

eissn

0002-9378

issn

1097-6868

pii

S0002937805002425

journal_volume

192

pub_type

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