Renal angiotensin-II receptors expression changes in a model of preeclampsia

The blunted response to angiotensin II (Ang II) during pregnancy is lost in patients by preeclampsia. This impaired response has been attributed to a change in one or both of the Ang II receptors, type 1 (AT1R) and type 2 (AT2R). The ratio of the Ang II receptor types in the kidney has not been studied. We postulated that an imbalance exists between AT1R/AT2R receptors in the renal cortex from rats subjected to an experimental model of preeclampsia, and that this altered ratio can modify the characteristic blunted pressor response to Ang II during pregnancy. The feto-placental units of Wistar rats were made ischemic by subrenal aortic coarctation, thus creating an experimental model of preeclampsia. We measured the AT1R and AT2R protein expression and the presence of the heterodimer AT1R/AT2R in the renal cortex and evaluated the pressor response to Ang II in an isolated kidney preparation from non-pregnant, healthy pregnant, and preeclampsia model rats. Pregnancy increased AT2R and AT1R/AT2R heterodimer expression and decreased the pressor response to Ang II. In contrast, AT1R increased, while AT2R and AT1R/AT2R heterodimer decreased in the preeclampsia model group. Thus, Ang II hypersensitivity observed in preeclampsia might be related to an increased expression of AT1R over AT2R and to a decreased presence of the AT1R/AT2R heterodimer in renal cortex.