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(Hypertension. 2008;52:44.)
© 2008 American Heart Association, Inc.

Brief Reviews

Developmental Programming of Hypertension

Insight From Animal Models of Nutritional Manipulation

Norma B. Ojeda; Daniela Grigore; Barbara T. Alexander

From the Department of Physiology, University of Mississippi Medical Center, Jackson.

Correspondence to Barbara T. Alexander, Department of Physiology, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 39216-4505. E-mail balexander@physiology.umsmed.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Low birth weight (LBW), defined as a birth weight of 2.5 kg at term, is a major health issue within the United States today. The risk for LBW is greater within the black population than the white, with a greater percentage of LBW occurring within the southern United States relative to other parts of the country.¹ Infants born small for gestational age not only have a greater risk for survival at birth^2,3 but, based on numerous epidemiological studies, face long-term consequences, such as increased risk for development of hypertension, cardiovascular disease, diabetes, and other health problems.^4–6 Barker⁷ first proposed that an adverse environmental stimulus experienced during a critical period of fetal development leads to slow fetal growth and permanent structural and physiological changes in the fetus predisposing it to increased risk for the development of hypertension and cardiovascular disease. Investigators using animal models to induce an adverse fetal environment and mimic the human condition of slow fetal growth are providing convincing evidence to support the concept of developmental programming of adult disease.^8–17 Although there is compelling epidemiological and experimental data that suggest that cardiovascular diseases such as hypertension may be programmed in utero, the underlying pathophysiological mechanisms remain unclear. Investigators use unique animal models of nutritional manipulation to induce slow fetal growth to examine the mechanisms linking birth weight and chronic adult disease, such as hypertension. In this review, we discuss alterations in potential mechanistic pathways that evolve in response to fetal insult and lead to the developmental programming of . . . [Full Text of this Article]

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