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Renal Development and Blood Pressure in Offspring from Dams Submitted to High-Sodium Intake during Pregnancy and Lactation

DOI: 10.1155/2012/919128

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Exposure to an adverse environment in utero appears to programme physiology and metabolism permanently, with long-term consequences for health of the fetus or offspring. It was observed that the offspring from dams submitted to high-sodium intake during pregnancy present disturbances in renal development and in blood pressure. These alterations were associated with lower plasma levels of angiotensin II (AII) and changes in renal AII receptor I (AT1) and mitogen-activated protein kinase (MAPK) expressions during post natal kidney development. Clinical and experimental evidence show that the renin-angiotensin system (RAS) participates in renal development. Many effects of AII are mediated through MAPK pathways. Extracellular signal-regulated protein kinases (ERKs) play a pivotal role in cellular proliferation and differentiation. In conclusion, high-sodium intake during pregnancy and lactation can provoke disturbances in renal development in offspring leading to functional and structural alterations that persist in adult life. These changes can be related at least in part with the decrease in RAS activity considering that this system has an important role in renal development. 1. Introduction The risk of hypertension, renal, and cardiovascular disease are in part determined before birth by intrauterine factors. Exposure to an adverse environment in utero appears to programme physiology and metabolism permanently, with long-term consequences for health of the fetus or offspring [1, 2]. The nephrogenesis in rats begins on embryonic day 12 and is completed at between 10 and 15 days after birth [3, 4]. Clinical and experimental evidence show that the renin-angiotensinn system (RAS) participates in renal development [5–11]. In the rat kidney, angiotensinogen expression is higher during the late gestation and newborn period whilst renin mRNA is detected from embryonic day 17 and is higher on embryonic day 20 and in newborns compared to adults [7, 8]. Renal AII content is several fold higher in newborn rats and mice than in their adult counterparts. The AII receptors are also expressed to a greater degree in newborn rats [9]. The mRNA for the type 1 AII receptor (AT1) has been detected in the renal glomeruli of newborn rats during cellular proliferation and differentiation [10]. Increase in fibronectin, -SM-actin ( -smooth muscle actin), PCNA (proliferating cell nuclear antigen) and p-ERK (extracellular signal-regulated protein kinase) expressions were observed in the renal cortex of 1- and 7-day-old rats, followed by a decrease during renal development [12].

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