Anguiano-Robledo Liliana, Reyes-Melchor Pedro A, Bobadilla-Lugo Rosa A, Pérez-Alvarez Víctor M, López-Sánchez Pedro
Escuela Superior de Medicina del IPN, Plan de San Luis y Diáz Mirón, Casco de Santo Tomás, México.
Hypertens Pregnancy. 2007;26(2):151-61. doi: 10.1080/10641950701252827.
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.
子痫前期患者孕期对血管紧张素II（Ang II）的反应减弱。这种反应受损归因于Ang II 1型受体（AT(1)R）和2型受体（AT(2)R）中一种或两种的变化。尚未对肾脏中Ang II受体类型的比例进行研究。我们推测，子痫前期实验模型大鼠的肾皮质中AT(1)R/AT(2)R受体之间存在失衡，且这种改变的比例可改变孕期对Ang II特征性的血压反应减弱。通过腹主动脉缩窄使Wistar大鼠的胎儿 - 胎盘单位缺血，从而建立子痫前期实验模型。我们测量了肾皮质中AT(1)R和AT(2)R蛋白表达以及AT(1)R/AT(2)R异二聚体的存在情况，并评估了非妊娠、健康妊娠和子痫前期模型大鼠离体肾脏制剂对Ang II的血压反应。妊娠增加了AT(2)R和AT(1)R/AT(2)R异二聚体的表达，并降低了对Ang II的血压反应。相比之下，子痫前期模型组中AT(1)R增加，而AT(2)R和AT(1)R/AT(2)R异二聚体减少。因此，子痫前期中观察到的Ang II超敏反应可能与肾皮质中AT(1)R表达高于AT(2)R以及AT(1)R/AT(2)R异二聚体的存在减少有关。
