The Impact of Nutritional Insults during Fetal Life on Blood Pressure

J Nutr Sci Vitaminol (Tokyo). 2015:61 Suppl:S5-6. doi: 10.3177/jnsv.61.S5.

Abstract

Numerous epidemiological and experimental studies provide compelling evidence that nutritional insults that impact fetal growth program a marked increase in blood pressure in later life. Sex and age also influence the developmental programming of hypertension; yet the exact mechanisms that permanently change the structure, physiology, and endocrine health of an individual across their lifespan following exposure to a nutritional insult are not entirely clear. Fetal exposure to maternal glucocorticoids is postulated as an initiating event. In addition, inappropriate suppression or activation of the renin angiotensin system (RAS) and/or activation of the sympathetic nervous system (SNS) leading to marked increases in oxidative stress and endothelin production are implicated in the etiology of hypertension that has its origins in fetal life. The risk of hypertension and chronic disease in one generation is transmitted to the next in the absence of an additional prenatal insult implicating epigenetic processes. Yet, further studies are needed to fully elucidate the mechanisms that contribute to hypertension programmed in response to nutritional insults during early life in order to improve the cardiovascular health of an individual across their lifespan.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Pressure*
  • Endothelins / metabolism
  • Female
  • Fetal Development*
  • Glucocorticoids / metabolism
  • Humans
  • Hypertension / etiology
  • Hypertension / physiopathology
  • Infant, Low Birth Weight
  • Malnutrition / complications
  • Malnutrition / physiopathology
  • Maternal Nutritional Physiological Phenomena*
  • Nutritional Status*
  • Oxidative Stress
  • Renin-Angiotensin System / physiology
  • Sympathetic Nervous System / metabolism

Substances

  • Endothelins
  • Glucocorticoids