Role of Fetal Programming in the Development of Hypertension

Abstract

Epidemiological studies have suggested that size at birth contributes to increased cardiovascular disease (CVD) risk in later life. Findings from experimental studies are providing insight into the mechanisms linking impaired fetal growth and the increased risk of CVD and hypertension in adulthood. This article summarizes potential mechanisms involved in the fetal programming of hypertension and CVD, including alterations in the organs and regulatory systems critical to long-term control of sodium and volume homeostasis.

Keywords: :

• glucocorticoids
• kidney
• renin–angiotensin system
• sex hormones
• sympathetic nervous system
• vascular function

Financial & competing interests disclosure.

Barbara Alexander is supported by the NIH grants HL074927 and HL51971. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.