Subjects formerly born preterm subsequently develop arterial - particularly isolated systolic-
hypertension more frequently than their peers born at term.
Numerous factors may influence this predisposition, including an incomplete nephrogenesis, implying
the presence of kidneys with a reduced number of nephrons and consequent reduction in haematic
filtration, increased sodium absorption and activation of renin-angiotensin-aldosterone system,
increased arterial rigidity produced by an elastin deficiency previously observed in anatomic
specimens of human immature aorta, and reduced endothelial nitric oxide excretion, due to high
blood levels of ADMA, a strong direct inhibitor of nitric oxide that exerts a vasoconstrictor effect.
Other possible factors (i.e. excretion of neuroendocrine compounds) may also be implicated. The
aim of this paper was to review all possible mechanisms involved in the observed increase in blood
pressure in individuals who had been born preterm and/or with intrauterine growth restriction. The
outlook for new and promising laboratory techniques capable of identifying alterations in the metabolic
pathways regulating blood pressure levels, such as metabolomics, is also provided.