The influence of vasopressin on the passage of tritiated water through the isolated amniotic membrane and other tissues from the fetal guinea pig

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Abstract
Amniotic membranes from fetal guinea pigs (0.62–1.00 of term), were kept in a continuous-flow perfusion cell. Vasopressin (50–500 mU/ml; fetal surface) increased the unidirectional maternal–fetal flux of 3H2O by up to 12.3 ± 1.5%. The corresponding reverse flux increased only 1.6%. The responses in the maternal–fetal direction showed a linear relationship with the log dose of vasopressin. Over the same period (35 min), there was a 13.6 ± 6.3% increase in the maternal–fetal flux of 22Na+. Therefore, vasopressin may influence water movement by an effect on ions, such as Na+ or Cl−.Isolated midterm fetal skin showed closely similar effects; vasopressin (500–1000 mU/ml; outer surface) increased the amniotic–fetal flux of 3H2O by up to 30.4 ± 13.7%. The late-term fetal bladder responded to vasopressin (100 mU/ml; outer, serosal surface), by increasing the flux of 3H2O from lumen to fetus by 49.4 ± 17.8%; one bladder showed a transient rise close to 85%.The sensitivities of the skin and amnion were similar, but the bladder was about 12 times more sensitive to vasopressin. The possibility that vasopressin influences an extraplacental route for the supply of water to the fetus, through the amnion, skin, and bladder, is suggested.