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 (AT(1)R) and type 2 (AT(2)R). The ratio of the Ang II receptor types in the kidney has not been studied. We postulated that an imbalance exists between AT(1)R/AT(2)R 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 AT(1)R and AT(2)R protein expression and the presence of the heterodimer AT(1)R/AT(2)R 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 AT(2)R and AT(1)R/AT(2)R heterodimer expression and decreased the pressor response to Ang II. In contrast, AT(1)R increased, while AT(2)R and AT(1)R/AT(2)R heterodimer decreased in the preeclampsia model group. Thus, Ang II hypersensitivity observed in preeclampsia might be related to an increased expression of AT(1)R over AT(2)R and to a decreased presence of the AT(1)R/AT(2)R heterodimer in renal cortex.