自主皮质醇分泌促进血管化在体内和体外在超阿尔多斯特主义下
Bo-Ching Lee1,2,3, Chin-Chen Chang1, Victor Jing-Wei Kang1
1Departments of Medical Imaging, National Taiwan University College of Medicine, Taipei, Taiwan, ROC.
概括
在原发性阿尔多斯特龙症 (PA) 患者中,自主皮质醇分泌 (ACS) 与增加腹腔大动脉化 (AAC) 有关. 皮质醇和阿尔多激素通过矿物质皮质醇受体信号来协同促进血管化,而eplerenone可以减少这种信号.
科学领域:
- 内分泌学 在内分泌学.
- 心血管医学 心血管医学
- 病理生理学 病理生理学
背景情况:
- 自主皮质醇分泌 (ACS) 是已知的原发性阿尔多斯 (PA) 的并发症.
- 在PA中失调的皮质醇分泌对心血管的影响,特别是对血管化的影响,尚不清楚.
- 了解这种关系对于管理PA患者心血管风险至关重要.
研究的目的:
- 研究PA患者中ACS和血管化之间的关联.
- 探索体外和体外的机制,通过这些机制ACS影响血管化在hyperaldosteronism的背景下.
主要方法:
- 对339名上腺瘤患者的回顾性分析,评估腹腔大动脉化 (AAC) 评分.
- 在体外研究中使用人类大动脉光滑肌细胞 (HAOSMCs) 来建模血管化.
- 多变量分析以确定AAC的独立预测因子和涉及矿物质皮质体受体 (MR) 抗剂的机制研究.
主要成果:
- 与没有ACS的患者相比,患有PA和ACS的患者的AAC得分显著更高.
- ACS与AAC分数的增加独立相关,抑制后的皮质醇水平与化严重程度相关.
- 在体外,皮质醇和阿尔多斯特协同增加了性酸酶活性和HAOSMC中的沉积,由MR信号介导.
结论:
- 自主皮质醇分泌与原发性阿尔多斯特症患者更严重的血管化有关.
- 阿尔多和皮质醇通过矿物质皮质醇受体信号协同作用,促进光滑肌肉细胞中的血管化.
- 矿物质皮质类受体对手eplerenone证明了减弱这种协同化过程的潜力.
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