Relative Concentrations of Placental Lactogen II and PRL-Like Protein-A in Stressed Rats Placenta

Abstract

The chronic stress induces functional adaptations in the hypothalamo-pituitary-adrenocortical (HPA) and in the sympathetic-medullary-adrenal axis (SAM). Both axis are considered vital regulators of the homeostasis in vertebrates (Seyle, 1936; Ostrandrer et al., 2006. On the other hand, the placenta provides highly specialized functions during gestation that are critical for the normal development of the embryo/fetus (Soares et al., 1991). We hypothesized that the chronic immobilization (IMO) stress in pregnancy rats produces alterations in prolactin concentrations in placental tissue and also changes in the response of SAM axis. Chronic stress by IMO was applied on days 12, 17 and 21 of pregnancy rats. Relative concentrations and localization of placental lactogen-II (PL-II) and the PRL-like protein A (PLP-A) in chorioalantoic placenta were estimated by Immunoblotting and Immunocytochemical analysis. The levels of catecholamines metabolite, acid 3-metoxi 4-hidroximandélico (VMA), were analyzed in stressed rats urines on 6,12,17,21 days of pregnancy, by HPLC, in order to determine the response of SAM axis. During the days of the pregnancy studied, chronic stress did not induce any changes neither in the localization nor in placental concentrations of PL-II and PLP-A. The VMA values in stressed mothers urines increased on the day 6 respecting the control ones at the same time of pregnancy. VMA values in stressed rats at 21 days of pregnancy are smaller than the respective controls. 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.

Attenuation effects of prenatal stress by early postnatal stimulation in different research models

“…There are evidences that elevated levels of circulating maternal catecholamines could impair fetal development indirectly through placental vasoconstriction that reduces oxygen and nutrient supply to the fetus/es. 19,20 Romanini et al 21 concluded that the chronically stressed rats had activated the sympathetic-medullaryadrenal axis and increased the levels of catecholamine metabolite, acid 3-metoxi 4-hidroximandélico, in urines at the beginning of pregnancy. Also, high concentrations of corticotropin-releasing hormone (CRH) are found in growth-retarded fetuses and elevated maternal CRH levels are associated with decreased gestational length and increased risk of preterm delivery.…”

“…Table 1 summarizes the effect of prenatal stress and postnatal handling on selected endocrine and immune physiological parameters. 70 Lesage et al 15 Macrís et al 56 Romanini et al 21 Liaudat et al 43 Mayer et al 26 Desplats et al 71 Schroeder et al 28 Adrenal 70 Maccari et al 34 Meaney et al 55 Weinstock et al 69 McCormick et al 77 Smythe et al 70 Fenoglio et al 60 Total leucocytes ↓ Mayer et al 26 ↑ Liaudat et al 43 Liaudat et al 43 Llorente et al 78 Dhabbar et al 79 Lymphocytes number ↓ Llorente et al 78 ↑ Liaudat et al 43…”