کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3006084 | 1180954 | 2012 | 9 صفحه PDF | دانلود رایگان |

The etiology of preeclampsia remains unknown. However, a contributing factor to this hypertensive disease of pregnancy is a reduction in uterine perfusion pressure resulting in placental ischemia. Uterine arteries may be a major regulator of this process through changes in vascular reactivity and localized blood flow. The reduced uterine perfusion pressure (RUPP) pregnant rat is an established animal model of preeclampsia pathology. Pregnant Sprague Dawley rats were used for this investigation and subjected to RUPP or SHAM surgery on Day 14 of gestation. On Day 21 of gestation, animals were terminated and resistance-caliber uterine arteries were harvested and mounted on a pressurized arteriograph to examine myogenic reactivity, agonist induced vasodilation (methacholine and VEGF), and vasoconstriction (phenylephrine and U-46619). Resistance-caliber uterine arteries from RUPP animals exhibited increased myogenic reactivity and decreased vasodilation (methacholine and VEGF) compared to SHAM uterine arteries (p < 0.05). Phenylephrine and U-46619 induced constriction was similar in uterine arteries between RUPP and SHAM rats. These results suggest that resistance-caliber uterine arteries from RUPP pregnant rats are altered to reflect a more constrictive phenotype which may play a role in the development of maternal hypertension demonstrated in these animals and thereby potentially in preeclampsia.
Journal: Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health - Volume 2, Issue 2, April 2012, Pages 106–114