Angiotensin II (Ang II) evoked secretion of the human placental lactogen (HPL) in intrauterine growth retardation: examination of the relationship with Ang II receptor type 1 (AT1) expression.

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.