Abstract
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.
Original language | English (US) |
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Pages (from-to) | 507.e1-507.e10 |
Journal | American journal of obstetrics and gynecology |
Volume | 206 |
Issue number | 6 |
DOIs | |
State | Published - Jun 2012 |
Externally published | Yes |
Keywords
- angiotensin
- fetal programming
- hypertension
- intrauterine growth restriction
- rats
- vascular
ASJC Scopus subject areas
- Obstetrics and Gynecology