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1 Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States; Physiology, University of Mississippi Medical Center, Jackson, Mississippi, United States
2 Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States
* To whom correspondence should be addressed. E-mail: balexander{at}physiology.umsmed.edu.
Our laboratory utilizes a model of intrauterine growth restriction (IUGR) induced by
placental insufficiency in the rat to examine the developmental origins of adult disease. In this model only male IUGR offspring remain hypertensive in adulthood, revealing sex specific differences. The purpose of this study was to determine whether testosterone with participation of the renin angiotensin system (RAS) contributes to hypertension in adult male IUGR offspring. At 16 weeks of age a significant increase in testosterone (346±34 vs. 189±12 ng/dl, P<0.05) was associated with a significant increase in mean arterial pressure (MAP) measured by telemetry in IUGR offspring (147±1 vs. 125±1 mmHg, P<0.05, IUGR vs. control, respectively). Gonadectomy (CTX) at 10 weeks of age significantly reduced MAP by 16 weeks of age in IUGR offspring (124±2 mmHg, P<0.05 vs. intact IUGR), but had no effect in control (125±2 mmHg). A significant decrease in MAP in intact IUGR (111±3 mmHg, P<0.05 vs. untreated intact IUGR) and
castrated IUGR (110±4 mmHg, P<0.05 vs. untreated CTX IUGR) after treatment with enalapril for 2 weeks suggests a role for RAS involvement. However, the decrease in blood pressure in response to enalapril was greater in intact IUGR (
36±1 mmHg, P<0.05) compared to CTX IUGR ( 15±2 mmHg) indicating an enhanced response to RAS blockade in the presence of testosterone. Thus, these results suggest that testosterone plays a role in modulating hypertension in adult male IUGR offspring with participation of the RAS.
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