Developmental programming and hypertension.
OBJECTIVE
There is a growing body of evidence linking adverse events or exposures during early life and adult-onset diseases. After important epidemiological studies from many parts of the world, research now focuses on mechanisms of organ dysfunction and on refining the understanding of the interaction between common elements of adverse perinatal conditions, such as nutrition, oxidants, and toxins exposures. This review will focus on advances in our comprehension of developmental programming of hypertension.


RESULTS
Recent studies have unraveled important mechanisms of oligonephronia and impaired renal function, altered vascular function and structure as well as sympathetic regulation of the cardiovascular system. Furthermore, interactions between prenatal insults and postnatal conditions are the subject of intensive research. Prematurity vs. intrauterine growth restriction modulate differently programming of high blood pressure. Along with antenatal exposure to glucocorticoids and imbalanced nutrition, a critical role for perinatal oxidative stress is emerging.


CONCLUSIONS
While the complexity of the interactions between antenatal and postnatal influences on adult blood pressure is increasingly recognized, the importance of postnatal life in (positively) modulating developmental programming offers the hope of a critical window of opportunity to reverse programming and prevent or reduce related adult-onset diseases.
Nuyt
Anne Monique
AM
Department of Pediatrics, Research Center, CHU Sainte-Justine, Université de Montréal, Canada. anne-monique.nuyt@recherche-ste-justine.qc.ca
Alexander
Barbara T
BT
D000818:Animals; D001724:Birth Weight; D001808:Blood Vessels / Q000473:pathology / Q000502:physiology; D004198:Disease Susceptibility; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D005333:Fetus / Q000187:drug effects; D005938:Glucocorticoids / Q000494:pharmacology; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000209:etiology*; D007668:Kidney / Q000294:innervation; D023421:Models, Animal; D009399:Nephrons / Q000502:physiology; D011247:Pregnancy; D047928:Premature Birth / Q000503:physiopathology; D039401:Prenatal Nutritional Physiological Phenomena; D017673:Sodium Chloride, Dietary / Q000494:pharmacology
D005938:Glucocorticoids; D012739:Gonadal Steroid Hormones; D017673:Sodium Chloride, Dietary