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A novel model of polyhydramnios: amniotic fluid volume is increased in aquaporin 1 knockout mice
Stephanie E Mann1, Emily A Ricke, Elvina A Torres
1Department of Obstetrics, Gynecology, and Reproductive Sciences and Medicine, University of California, San Francisco, USA. Stephanie_mann@medprodoctors.com
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.
