Mineralocorticoid receptor blockade attenuates proliferative changes in the rat pulmonary artery in monocrotaline-induced pulmonary hypertension

本研究旨在探讨盐皮质激素受体（MR）信号通路在肺动脉高压（PAH）小动脉重构中的作用。雄性大鼠单次皮下注射野百合碱诱导PAH。将动物分为两组：一组口服MR拮抗剂治疗，另一组不接受药物治疗。MR拮抗剂治疗改善了无药物组中由RV峰值压力升高引起的RV功能降低和肥大。与未用药组相比，治疗组显示PA的中壁厚度和肌化显著减少。MR拮抗剂治疗导致肺组织中MR、血管紧张素2 1a型受体和转化生长因子β 1的mRNA水平显著降低，这些结果表明MR信号在PAH的增殖性血管重塑中起作用。

The aim of this study was to investigate a role of mineralocorticoid receptor (MR) signaling in the arteriolar remodeling of pulmonary artery hypertension (PAH) by antagonizing MR.PAH was induced by a single subcutaneous injection of monocrotaline in male rats. Animals were divided in two groups: one group treated with oral MR antagonist and the other received no medication. MR antagonist treatment ameliorated increased reduced RV function and hypertrophy caused by elevated peak RV pressure seen in the group with no medication. The treatment group showed significantly less medial wall thickness and muscularization of PA compared to the group with no medication. MR antagonist treatment resulted in significant reduction in the mRNA levels of the MR, angiotensin 2 type 1a receptor and transforming growth factor beta1 in the lungs, when compared to the group with no medication.These results suggest that MR signaling plays a role in the proliferative vascular remodeling of PAH.