Preeclampsia (PE) is a hypertensive complication of pregnancy. Its cause is still unknown and it could be a risk factor for future ophthalmic problems. Retinal vascular bed alterations have been described as a consequence of PE, suggesting a retinopathy. Factors related to angiogenesis and vascular permeability, such as vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) or components of the renin angiotensin aldosterone system (RAAS), prorrenin/renin receptor ((P)RR) and angiotensin II type I receptor (AT1R) have been located in the retina, participating in other retinopathies, but it is unknown if they could participate in PE. Our aim was to elucidate whether VEGF, PEDF, (P)RR and AT1R could be modified during PE and during hypertension induced in rats with a history of PE. We used female Wistar rats and subrrenal aortic coarctation to induce PE, and after delivery, we induced a second hit by Nω-nitro-L-arginine methyl ester (L-NAME) administration. We measured blood pressure, proteinuria and pups development. In both models, eye fundal exploration and immunoblot for VEGF, PEDF, (P)RR and AT1R were performed. We found that the development of hypertension occurred faster in previously PE rats than in normal animals. VEGF, PEDF, (P)RR and AT1R were increased in PE, but in L-NAME-induced hypertension only (P)RR and AT1R were altered. Eye fundal data indicated that PE induced a level I retinopathy, but L-NAME induced a faster and more severe retinopathy in previously PE animals compared to previously normal pregnancy rats. These results indicate that PE predisposes to development of a faster and more severe retinopathy after a second hit. They also suggest that VEGF and PEDF seem to participate only in PE retinopathy, but in both models, RAAS components seem to have a more critical participation.

中文翻译：

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子痫前期是高血压性视网膜病的诱发因素：RAAS的参与和血管生成因子。

子痫前期（PE）是妊娠高血压并发症。其原因仍然未知，并且可能是未来眼科疾病的危险因素。视网膜血管床改变已被描述为PE的结果，提示视网膜病变。与血管生成和血管通透性相关的因素，例如血管内皮生长因子（VEGF）和色素上皮衍生因子（PEDF）或肾素血管紧张素醛固酮系统（RAAS），肾上腺素/肾素受体（（P）RR）和血管紧张素II的成分I型受体（AT1R）位于视网膜中，参与其他视网膜病变，但尚不清楚它们是否可以参与PE。我们的目的是阐明在有PE史的大鼠中，在PE和高血压期间是否可以修饰VEGF，PEDF，（P）RR和AT1R。我们使用雌性Wistar大鼠和肾下主动脉缩窄诱导PE，分娩后，我们通过Nω-硝基-L-精氨酸甲酯（L-NAME）给药诱导了第二次发作。我们测量了血压，蛋白尿和幼崽的发育。在这两种模型中，均进行了眼底探查和VEGF，PEDF，（P）RR和AT1R的免疫印迹。我们发现先前的PE大鼠中高血压的发生比正常动物中的发生更快。PE中VEGF，PEDF，（P）RR和AT1R升高，但是在L-NAME诱发的高血压中，仅（P）RR和AT1R发生了改变。眼底数据表明，与先前的正常妊娠大鼠相比，先前的PE动物诱发了I级视网膜病变，但L-NAME诱发了更快，更严重的视网膜病变。这些结果表明，PE容易在第二次发作后发展为更快，更严重的视网膜病变。他们还表明，VEGF和PEDF似乎仅参与PE视网膜病变，但在这两种模型中，RAAS组分似乎都具有更关键的参与。