ALTERED VASOREGULATION IN PORTAL HYPERTENSION

门静脉高压症（PHT）及其并发症占全球10万以上， 美国的死亡人数，使其成为四大原因之一， 死亡由于我们缺乏对改变的病因学的了解， 在PHT的血管调节中，治疗并不针对逆转这些 异常这项提案将确定受体和G蛋白- 一氧化氮介导的相关信号机制改变， 前列环素，这两种肽激素被认为是最主要的原因。 PHT血管充血。增加的剪切力 压力和/或压力以及PHT中改变的血管调节也将 进行评估。将使用PHT的大鼠模型，连同血管内皮细胞。 静态培养和VSMG共培养中的平滑肌细胞（VSMC），和 内皮细胞暴露于可变的剪切应力和/或压力。这些 实验应该提供有价值的信息， 了解PHT和其他血管性高血压的血管调节 事件

Portal hypertension (PHT) and its complications account for over 100,000 deaths in the United States, making it one of the top four causes of death. Due to our lack of understanding of the etiology of the altered vasoregulation in PHT, treatment has not been directed at reversing these abnormalities. This proposal will determine the receptor and G-protein- linked signal mechanism alterations mediated by nitric oxide and prostacyclin, the two peptide hormones judged most responsible for the vascular hyperemia of PHT. The relationship between increased shear stress and/or pressure and the altered vasoregulation in PHT will also be assessed. A rat model of PHT will be used, together with vascular smooth muscle cells (VSMC) in static culture and co-cultures of VSMG, and endothelial cells exposed to variable shear stress and/or pressure. These experiments should provide valuable information central to our understanding of PHT and vasoregulation in other vascular hypertensive events.