Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 287, Issue 5, Pages E863-E870Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00137.2004
Keywords
glucocorticoids; birth weight; hypothalamic-pituitary axis; glucose homeostasis; blood pressure; renin-angiotensin system
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Glucocorticoid overexposure in utero may underlie the association between low birth weight and subsequent development of common cardiovascular and metabolic pathologies. Previously, we have shown that prenatal dexamethasone (DEX) exposure in rat reduces birth weight and programs the hypothalamic-pituitary axis and fasting and postprandial hyperglycemia in adult males and hypertension in adult males and females. This study aimed to determine 1) whether there were gender differences in prenatal DEX-programmed offspring, and 2) whether the renin-angiotensin system (RAS) plays a role in the programming of hypertension. Rats exposed to DEX in utero (100 mug.kg(-1).day(-1) from embryonic days 14-21) were of lower birth weight (by 12%, P<0.01) and displayed full catch-up growth within the first month of postnatal life. DEX-treated male offspring in adulthood selectively displayed elevated plasma adrenocorticotropic hormone (by 221%) and corticosterone (by 188%, P<0.05), postprandial insulin-glucose ratios (by 100%, P<0.05), and hepatic expression of the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (by 38%, P<0.05). Conversely, DEX-programmed females were hypertensive (by 11%, P<0.05), with elevated hepatic angiotensinogen mRNA expression (by 9%, P<0.05), plasma angiotensinogen (by 61%, P<0.05), and renin activity (by 88%, P<0.05). These findings demonstrate that prenatal glucocorticoids program adulthood cardiovascular and metabolic physiology in a gender-specific pattern, and that an activated RAS may in part underlie the hypertension associated with prenatal DEX programming.
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