Retinal vasculature in hypertension

大约32%-44%的美国成年人口患有高血压，并伴有多种并发症之一 患有高血压视网膜病变。在一项研究中，视网膜病变的患病率被发现在 重度高血压者占25%，轻度高血压者占25%。视网膜损害的后果 高血压包括小动脉狭窄、出血、棉花斑(局限性缺氧)和视神经。 椎间盘肿胀。其他视网膜改变包括小动脉壁玻璃化、血管增厚。 基底膜、毛细血管闭合、平滑肌变性和血-视网膜屏障 功能障碍。此外，高血压是视网膜动脉高度危险事件的主要危险因素。 或静脉闭塞。高血压视网膜病变的主要治疗方法是降低血压；然而， 这种疾病的后果包括小动脉变窄，即使在降压治疗后仍然存在。 药物治疗。因此，对疾病机制的更好了解可能会导致这种疾病的发展 更多和更有效的治疗选择。我们的总体假设是血管 高血压性视网膜病变的并发症是内皮和平滑肌的表型改变 细胞，即使使用降压药，血管壁重塑也会限制恢复。具体的 目的是：(1)确定视网膜中糖萼的性别依赖性表达，并确定 高血压对这一表达的影响，(2)检测血小板的性别依赖性表达 视网膜中的内皮细胞黏附分子-1和血管内皮细胞钙粘附素，并检验假说 高血压视网膜中这些连接分子的变化是由于内皮细胞到血管内皮细胞 间充质转化，以及(3)检验自发性高血压大鼠视网膜血管壁重塑的假设 当高血压降至正常时，会导致视网膜血流灌注不良。

Approximately 32-44% of the adult US population has hypertension, with one of the many complications being hypertensive retinopathy. In one study, the prevalence of retinopathy was found to be 85% amongst those with severe hypertension, and 25% for those with mild hypertension. Retinal consequences of hypertension include arteriolar narrowing, hemorrhages, cotton wool spots (localized hypoxia), and optic disk swelling. Other retinal changes include hyalinization of arteriolar walls, thickening of the vascular basement membrane, closure of capillaries, smooth muscle degeneration, and blood-retinal barrier dysfunction. Additionally, hypertension is a major risk factor for the highly threatening events of retinal artery or vein occlusion. The primary treatment for hypertensive retinopathy is to reduce blood pressure; however, consequences of the disease including narrowing of arterioles persist even following anti-hypertension medication. Therefore, a better knowledge of the mechanisms of the disease could lead to the development of additional and more effective therapeutic options. Our overall hypothesis is that the vascular complications of hypertensive retinopathy are due phenotypic changes in endothelial and smooth muscle cells, with vessel wall remodeling limiting recovery even with anti-hypertensive medication. The specific aims are to: (1) determine the sex-dependent expression of the glycocalyx in the retina, and determine the consequences of hypertension on this expression, (2) examine the sex-dependent expression of platelet endothelial adhesion molecule-1 and vascular endothelial cadherin in the retina, and test the hypothesis that changes in these junctional molecules in the hypertensive retina are due to endothelial-to- mesenchymal transition, and (3) test the hypothesis that remodeling of blood vessel walls in the SHR retina induces susceptibility to poor retinal perfusion when high blood pressure is reduced to normal.