Fetal origins of adult hypertension: a renal mechanism?

Abstract

It is well-recognized that the etiology of cardiovascular disease includes at least two components: a genetic component and a 'lifestyle' or environmental component. However, epidemiological evidence accumulating over the past decade has provided an increasingly strong case for the important involvement of a third component, that of environmental conditions during development (i.e. before birth), in contributing to an individual's overall cardiovascular risk. Factors in the prenatal environment to which a baby is exposed can cause permanent changes in the structure and function of specific tissues in the body. Although perhaps valuable in the short term in that they allow survival until birth, these changes are maladaptive in the long term because they predispose the individual to an array of adult diseases. Experimental data elucidating the possible physiological and morphological mechanisms by which this perinatal 'programming' for adult cardiovascular disease occurs are only just now becoming available. However, it appears that the renin-angiotensin system, and the important role it plays in renal development, may be central in setting the trajectory that leads to cardiovascular disease, and in particular hypertension.