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The influence of vasopressin and prolactin on the movement of water and sodium through the isolated amnion of the fetal guinea-pig Holt, William Faulkner


Unidirectional flux of tritiated water across isolated guinea-pig amnion was studied in a perfusion cell supplied with amniotic saline at 37° C by means of a continuous double-circulation system. The diffusional permeability in the absence of an osmotic gradient was 3.09 ± 0.15 x 10⁻⁴ cm sec⁻¹ for maternal-fetal flow (10 experiments), and 2.62 ± 0.14 x 10⁻⁴ cm sec⁻¹ for fetal-maternal flow (13 experiments). The addition of vasopressin (50-500 mU/ml) to the fetal side of sixteen membranes set up between amniotic and maternal salines increased isotopic water flux in the maternal-fetal direction against an osmotic gradient of 28 mOsm/l. Treatment of eight other membranes with 10 μg/ml prolactin reduced fetal-maternal water flow by up to 17.0 % at the end of 3 hours, in the absence of an osmotic gradient. This contrasted with five control experiments, in which fetal-maternal flow increased by 5.1 % at the end of 3 hours. Therefore, the prolactin appeared to reduce diffusional fetal-maternal water flow by up to 22.1 % within 3 hours. In twelve further experiments, net flow (fetal-maternal) was measured gravimetrically. The membranes were set up between amniotic and maternal salines, in conditions which paralleled the natural ionic environment, and the natural hydrostatic and osmotic gradients. In five experiments, the addition of prolactin (20 μg/ml) to the fetal surface of the amnion, caused a decrease in fetal-maternal water flow of almost 60 % at 3 hours. In contrast, seven control studies showed no such effects. Permeability of isolated amnion to sodium was studied over the course of gestation by the use of radioactive sodium (²²NaCl). Maternal-fetal sodium movement was found to increase by a factor of about 35 fold from day 57 to day 70. The treatment of membranes with vasopressin (500 mU/ml) produced an average decrease in maternal-fetal sodium movement of 12.2 ± 7.8 % in the third hour (2 experiments). Thus, water movement in this direction did not seem to be coupled to sodium flux. When prolactin (10 μg/ml) was added to seven membranes, an increase in maternal-fetal sodium flux of 21.3 ± 8.3 % was recorded in the third hour. Control membranes, however, showed a similar increase of 21.3 ± 14.9 % in the third hour (7 experiments). Therefore, comparison of experimental and control preparations suggests that prolactin probably does not affect maternal-fetal sodium movement. In contrast to this, treatment of five other membranes with prolactin (10 μg/ml) produced an average increase in fetal-maternal sodium flux of 53.6 ± 10.1 % in the third hour. Since five control membranes showed an increase of only 15.1 ± 15.9 % in this same time period, prolactin seemed to be responsible for producing an overall increase of 38.5 % in unidirectional flux of sodium. Preliminary experiments indicate that neurohypophyseal hormone can stimulate an increase in unidirectional water flux across other fetal membranes and tissues. Vasopressin (100 mU/ml) increased water flow across the isolated fetal urinary bladder in the mucosal-serosal direction by 49.4 ± 17.7 % at the end of an hour (3 experiments); a control membrane showed an increase of only 9.7 %. The addition of vasopressin (500-1000 mU/ml) increased serosal-mucosal water movement across isolated fetal skin by up to 30 % in 60 minutes (4 experiments). At the present time the effects of vasopressin and prolactin on water and/or sodium movement across isolated amnion, fetal urinary bladder, and fetal skin must be regarded as pharmacological. It seems probable, however, that some of the responses may be physiological since high levels of hormone are found in fetal blood (i.e. vasopressin) and amniotic fluid (i.e. prolactin). This study suggests that hormonal regulation of fetal hydro-mineral metabolism may explain the enigma of how hydro-osmotic homeostasis is achieved in the intrauterine compartments.

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