Abstract
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.
Highlights
Review ArticleIt was observed that the offspring from dams submitted to high-sodium intake during pregnancy present disturbances in renal development and in blood pressure
The risk of hypertension, renal, and cardiovascular disease are in part determined before birth by intrauterine factors
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
Summary
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. 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
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