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1 Centre for Reproduction and Early Life, Division of Nutritional Biochemistry, University of Nottingham, Sutton Bonington Campus, Loughborough, LE12 5RD, United Kingdom
* To whom correspondence should be addressed. E-mail: simon.langley-evans{at}nottingham.ac.uk.
Animal models support human epidemiological studies in demonstrating a relationship between impaired fetal growth and risk of adult hypertension. Undernutrition during pregnancy exerts programming effects on the developing kidney and modulation of angiotensin receptor (ATR) expression has been observed persisting into adult life. Fetal overexposure to glucocorticoids is thought to be central to the nutritional programming of blood pressure and may act through an interaction with ATR expression. Pregnant female Wistar rats were fed a control (n=6) or low protein (MLP, n=17) diet throughout pregnancy. The glucocorticoid dependency of MLP effects was tested using metyrapone, an inhibitor of corticosterone synthesis. MLP fed rats were injected twicedaily with metyrapone, metyrapone plus corticosterone or vehicle over days 1-14 of pregnancy. At delivery all animals were fed standard laboratory chow. 4-week old MLPexposed offspring exhibited increased systolic blood pressure in comparison to controls (P<0.05), which proved glucocorticoid-dependent in males only. AT1R mRNA expression was independent of in utero dietary treatment. AT2R mRNA expression was down-regulated in MLP exposed females only (P<0.05), in a glucocorticoid-independent manner. Male offspring exhibited glucocorticoid-dependent hypertension with no modulation of renal ATR mRNA expression. In contrast, female offspring exhibited glucocorticoid-independent hypertension associated with reduced expression of renal AT2R mRNA. These data do not support the hypothesis that an interaction between glucocorticoid and ATR mRNA expression underlies the nutritional programming of blood pressure, but instead suggest two independent mechanisms acting in a sex-specific manner.
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