کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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6147087 | 1594945 | 2012 | 10 صفحه PDF | دانلود رایگان |

ObjectiveExamine temporal alterations in vascular angiotensin II receptors (AT1R and AT2R) and determine vascular response to angiotensin II in growth-restricted offspring.Study DesignOffspring of pregnant rats fed low-protein (6%) and control (20%) diet were compared.ResultsPrenatal 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 AT1aR 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.ConclusionPrenatal protein restriction increased vascular AT1R expression and vasoconstriction to angiotensin II, possibly contributing to programmed hypertension.
Journal: American Journal of Obstetrics and Gynecology - Volume 206, Issue 6, June 2012, Pages 507.e1-507.e10