Renal Angiotensin-II Receptors Expression Changes in a Model of Preeclampsia

Abstract

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.

Keywords:

• Pregnancy
• Kidney
• Preeclampsia
• Angiotensin-II
• Angiotensin receptors