The effect of prolactin on sodium flux through the isolated amniotic membrane of the guinea pig

Abstract

Amniotic membranes from fetal guinea pigs (0.46–0.87 of term) were maintained in a continuous-flow perfusion cell, with amniotic saline on both surfaces. Prolactin (10 μg/ml; fetal surface) increased the unidirectional diffusional flux of 22Na+ in the fetal–maternal direction (maximum, about 75%; average over 3rd h, 53.6 ± 10.1%). This increase was significant when compared with albumin controls (P < 0.05) and with the initial base-line fluxes (P < 0.01). Albumin controls showed no significant change from the base-line flux. Therefore, prolactin appeared to increase the unidirectional flux of sodium out of the potential amniotic cavity.One membrane, at term and overdue, failed to respond.Experiments on the reverse, maternal–fetal flux of 22Na+ showed no differences between membranes treated with prolactin or albumin. Therefore, prolactin had no effect on the unidirectional flux of sodium into the potential amniotic cavity.Sodium permeability rose dramatically in membranes close to birth or overdue; 22Na+ fluxes increased about 20-fold in both directions.Prolactin appears capable of causing a net movement of sodium through the amnion, out of the amniotic fluid. Also, it is able to slow the movement of water in the same direction. These factors, taken together, suggest a partial explanation for the maintenance of a hypotonic amniotic fluid.