OBJECTIVE: Examine temporal alterations in vascular angiotensin II receptors (AT1R and AT2R) and determine vascular response to angiotensin II in growth-restricted offspring. STUDY DESIGN: Offspring of pregnant rats fed low-protein (6%) and control (20%) diet were compared. RESULTS: Prenatal protein restriction reprogrammed AT1aR messenger RNA expression in male rats' mesenteric arteries to cause 1.7- and 2.3-fold increases at 3 and 6 months of age associated with arterial pressure increases of 10 and 33 mm Hg, respectively; however, in female rats, increased AT 1aR expression (2-fold) and arterial pressure (15 mm Hg) occurred only at 6 months. Prenatal protein restriction did not affect AT2R expression. Losartan abolished hypertension, suggesting that AT1aR plays a primary role in arterial pressure elevation. Vasoconstriction to angiotensin II was exaggerated in all protein-restricted offspring, with greater potency and efficacy in male rats. CONCLUSION: Prenatal protein restriction increased vascular AT1R expression and vasoconstriction to angiotensin II, possibly contributing to programmed hypertension.
- fetal programming
- intrauterine growth restriction
ASJC Scopus subject areas
- Obstetrics and Gynecology