Preterm birth (< 37 gestational weeks) reaches 10% of total births worldwide. Early exposure
to an ex utero environment can alter organogenesis and maturation in the newborn. This
early onset of events can further promote long-term developmental alterations and cardiovascular
disease risks. Mechanisms activated during preterm birth and promoting such cardiovascular alterations
have just recently been investigated. As a major candidate, the renin angiotensin aldosterone
system (RAAS) can be acutely altered during preterm birth and persistently activated in later life.
Further, RAAS alterations may occur as consequence of kidney and heart immaturity to promote
adaptive responses, suggesting a dual role of this system on fetal and neonatal organogenesis. Furthermore,
fetal or neonatal exposure to deleterious stress conditions can significantly impact on this
dual RAAS role, contributing to the establishment of hemodynamic and structural alterations. In
this review, clinical and experimental findings describing RAAS components and activation in
relationship with preterm birth are discussed. Further clinical and experimental investigations on
RAAS activation in the context of preterm birth are needed to better understand this dual role of
RAAS on early development and on programming of risks to cardiovascular diseases.
Keywords: Preterm birth, renin angiotensin aldosterone system, cardiovascular diseases, pregnancy complications, neonatal
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