We conclude that the chronic stressed mothers activated the SAM axis at the beginning of pregnancy and then they diminished the metabolites catecholamines that were interpreted as a stress adaptation coincident with normal concentrations of both placentary prolactines at this stage of the pregnancy.
Obtention of placentary homogenates to apply immunoblot technique.
(Bullock & Petrusz, 1983) immunochemistry technique was used to identify the cells that synthesize placentary prolactines PL-II and PLP-A.
The localization of both placentary prolactines coincided with Cambell et al.
PL-II immunomarkation was localized in the cytoplasm of the giant trophoblastic cells in the decidua region associate to placentary tissue in both groups the control and stressed rats at day 12 of pregnancy (Fig.
The effects of chronic stress applied to gestating mothers, on the concentrations of PL II in the placentary tissue at 12, 17 and 21 days of pregnancy, were analyzed using the immunoblot technique (Fig.
No significant statistical differences were observed between the mean values of the concentrations of PL-II between the placentary homogenates of stressed rats and control ones without treatment at days 12, 17 and 21 of pregnancy (Fig.
PLP-A concentrations in placentary tissue of rats chronically stressed were quantified.
Since this acid is one of the metabolites of catecholamines, it was evaluated in the urine of pregnant rats to relate these peripheric values to the results obtained from the different variables analyzed in placentary homogenates from mothers under the effects of chronic stress.
PL-II is first expressed in placentary JZ and the LZ which would favor its access to maternal blood and to fetal vessels.