A novel model of polyhydramnios: amniotic fluid volume is increased in aquaporin 1 knockout mice.
OBJECTIVE
To test the hypothesis that amniotic fluid volume is increased in aquaporin 1 knockout mice.


METHODS
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.
Mann
Stephanie E
SE
Department of Obstetrics, Gynecology, and Reproductive Sciences and Medicine, University of California, San Francisco, USA. Stephanie_mann@medprodoctors.com
Ricke
Emily A
EA
Torres
Elvina A
EA
Taylor
Robert N
RN
D000653:Amniotic Fluid / Q000502:physiology*; D000818:Animals; D051398:Aquaporin 1; D020346:Aquaporins / Q000235:genetics*; D005260:Female; D051379:Mice; D018345:Mice, Knockout; D008954:Models, Biological; D010920:Placenta / Q000502:physiology*; D006831:Polyhydramnios / Q000503:physiopathology*; D011247:Pregnancy
C496021:Aqp1 protein, mouse; D020346:Aquaporins; D051398:Aquaporin 1