Mechanisms involved in developmental programming of hypertension and renal diseases. Gender differences.
BACKGROUND
A substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may "program" susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases.


METHODS
This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults.


RESULTS
Developmental programming of several diseases is secondary to changes in different mechanisms inducing important alterations in the normal development of several organs that lead to significant changes in birth weight. The different diseases occurring as a consequence of an adverse environment during development are secondary to morphological and functional cardiovascular and renal changes, to epigenetic changes and to an activation of several hormonal and regulatory systems, such as angiotensin II, sympathetic activity, nitric oxide, COX2-derived metabolites, oxidative stress and inflammation. The important sex-dependent differences in the developmental programming of diseases seem to be partly secondary to the effects of sex hormones. Recent studies have shown that the progression of these diseases is accelerated during aging in both sexes.


CONCLUSIONS
The cardiovascular, renal and metabolic diseases during adult life that occur as a consequence of several insults during fetal and postnatal periods are secondary to multiple structural and functional changes. Future studies are needed in order to prevent the origin and reduce the incidence and consequences of developmental programmed diseases.
Analia Lorena
AL
Tomat
Francisco Javier
FJ
Salazar
D000818:Animals; D001724:Birth Weight; D044127:Epigenesis, Genetic; D005260:Female; D012739:Gonadal Steroid Hormones / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000196:embryology / Q000378:metabolism / Q000503:physiopathology*; D007674:Kidney Diseases / Q000196:embryology / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008659:Metabolic Diseases / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D011247:Pregnancy; D012084:Renin-Angiotensin System / Q000502:physiology; D012737:Sex Factors; D013564:Sympathetic Nervous System / Q000196:embryology / Q000254:growth & development / Q000503:physiopathology
D012739:Gonadal Steroid Hormones