肺动脉高压发病与炎症反应密切相关。我们前期研究发现激活TRPV1（transient receptor potential vanilloid type 1）能通过神经多肽途径引起血管的舒张反应。TRPV1还介导了神经源性炎症反应。但是TRPV1在肺动脉高压发病中的作用及其机制并不明确。本课题通过建立低氧性肺动脉高压小鼠模型，分别以药物阻断和基因敲除方法，以明确TRPV1在血管重构致肺动脉高压过程中的作用。并且测定不同神经多肽与炎症细胞因子水平的差异，观察炎症细胞侵润程度，分析各项指标与肺动脉血管重构程度的相关性，探讨TRPV1在肺动脉高压发病中的炎症相关机制。同时寻求采用何种激动剂激活TRPV1，产生最佳的抗炎症效应，抑制肺动脉血管重构过程。研究结果将有助于阐明TRPV1通过抗炎神经肽——生长抑素途径抑制炎症反应减轻血管重构致肺动脉高压发病中的作用及部分作用机制，为药物筛选提供新的靶点。

Inflammation has been identified as a central mediator of pulmonary hypertension progression. The mechanism is not clear. We revealed that stimulation of the transient receptor potential vanilloid type 1 (TRPV1) can induce the vasodilation in our previous study. It is related to the release of neuropeptides. Moverover, TRPV1 is intrinsically associated with neurogenic inflammation. However, the role and the possible mechanism of TRPV1 in the pathogenesis of pulmonary hypertension remain unknown. The animal model of hypoxia-induced pulmonary hypertension is made to study the role and possible mechanisms of TRPV1 in vascular remodeling and pulmonary hypertension by drug blockade or gene deletion. Then, we observe the different levels of neuropeptides and inflammatory mediators and the extent of inflammatory cells infiltration. We also study the relationship between the degree of vascular remodeling and each index in order to find the inflammatory mechanism of TRPV1 on the pathogenesis of hypoxia-induced pulmonary hypertension. At the same time, we want to find a good way to inhibit inflammatory responses and decrease the degree of vascular remodeling through stimulating TRPV1. This study will provide the evidence for the role of TRPV1 on the pathogenesis of vascular remodeling and pulmonary hypertension. It is related to the anti-inflammation mediated by the neuropeptides, somatostatin, released from sensory nerve terminals in response to activation of TRPV1. It may prompt future development of a new class of drugs for prevention and treatment of pulmonary hypertension via the new targets.