The Na -ATPase, a secondary pump in the proximal tubule, is only weakly responsive to angiotensin II in adult offspring exposed perinatally to high Na intake. We have investigated whether the offspring from mothers given 0.3 mol/L NaCl show an ineffective angiotensin II action to increase in blood pressure. It was hypothesized that functional alterations at adult life are associated with the number of angiotensin II-positive cells in the developing kidney, with increased oxidative stress in maternal/foetal organs, or with morphometrical changes in placentas. Wistar female rats were maintained on 0.3 mol/L NaCl in their drinking water from 20 days before conception until weaning. After weaning, some of the male offspring were treated with enalapril for 21 days. Glomerular filtration rate was recorded up to 210 days of age, when mean arterial pressure was measured after infusion of angiotensin II. To investigate the placenta and foetal kidneys, mothers on tap water or NaCl were also treated with alpha-tocopherol, pregnancy being interrupted on the 20th day. There were no changes in the number of cells positive for angiotensin II in the foetal kidney and unchanged lipid peroxidation in the placenta of offspring exposed to NaCl, but the intermediate trophoblast area in the junctional zone was increased, possibly reducing maternal-foetal exchange. Glomerular filtration rate was reduced and there was an attenuated effect of angiotensin II on elevation of blood pressure, which could be mediated by an elevated angiotensin II during early life, once these disturbances had been prevented by early and short-term treatment with enalapril.
Disturbances during intrauterine development are linked to fetal growth retardation and programming of diseases at adult life. Placental oxidative stress and placental impaired angiogenesis may be underlying mechanisms. It was investigated whether maternal inflammation, induced by lipopolysaccharides (LPS) elevates oxidative stress and affects vascular endothelial growth factor (VEGF) in placenta of rats. LPS was administered in pregnant Wistar rats at days 13, 15, 17 and 19 of pregnancy, accompanied or not by α‐tocopherol treatment during all pregnancy. At 20th day of gestation, fetal and placental weights were not affected by LPS, however placental and fetal hepatic lipid peroxidation was increased, as well as, placental and maternal hepatic reduced glutathione (GSH) levels were lowered. Moreover, LPS treatment increased VEGF and VEGF receptor type‐1 (VEGFR‐1) expression. Maternal α‐tocopherol treatment prevented lipid peroxidation changes induced by LPS, albeit it did not recover GSH levels or changed expressions of VEGF and VEGFR‐1. Thus, although LPS increases oxidative stress, it may increase placental angiogenesis. CAPES, CNPq and FACEPE.
Sodium overload during pregnancy compromises the renal function of offspring at adult life. In this work we investigated whether maternal sodium overload affects placental lipid peroxidation and type‐1 VEGF receptor (VEGFR‐1) in the placenta. Pregnant Wistar rats were maintained with sodium chloride 1.8%, instead drinking water, from 20 days before pregnancy until the 20th day of pregnancy. Part of them was treated with α‐tocopherol or tempol from the 1st day of pregnancy. Maternal sodium overload did not change the placental or hepatic fetal lipid peroxidation; however it decreased the expression of VEGFR‐1 in placental labyrinth. Treatment with α‐tocopherol or tempol prevented sodium overload‐induced reduction in placental expression of VEGFR‐1. Different from tempol, α‐tocopherol effect was accompanied by reduction of lipid peroxidation in maternal placenta and fetal liver. These findings indicate that intrauterine programmed renal dysfunction produced by sodium overload might be due to compromised placental angiogenesis that is not correlated to placental lipid peroxidation. CAPES, CNPq and FACEPE.
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