کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2542342 | 1122698 | 2008 | 5 صفحه PDF | دانلود رایگان |
Angiotensin II (Ang II) and its hemodynamic effects on placental vasculature mediated via Ang II receptor type 1 (AT1) may play significant role in intrauterine growth retardation (IUGR). Placental lactogen (HPL) production directly reflects placental function. We compared influence of Ang II on HPL production in normal and IUGR-complicated pregnancies and correlated this phenomenon with AT1 expression. Basal and Ang II-evoked HPL secretion was examined in perfused placental lobules using ELISA. After immunostaining of placental sections, AT1 expression was estimated using quantitative morphometry. Ang II increased HPL secretion. Ang II-evoked increase in HPL concentration in the perfusion fluid was 27.36 ± 6.4 (%, ± SEM) lower in IUGR (p < 0.05) compared to normal-course pregnancies. AT1 expression was significantly decreased in IUGR and was 78.12 ± 8.2 (%, ± SEM) of the mean value of controls. Demonstrating that Ang II-evoked secretion of HPL in preeclampsia-free IUGR is decreased and correlates with down-regulated expression of AT1, we present a new approach to the pathophysiology of IUGR.
Journal: International Immunopharmacology - Volume 8, Issue 2, February 2008, Pages 177–181