The purpose of this review was to discuss the role of sodium and inflammation in the pathophysiology of hypertension and the observed different hemodynamic effects of drugs. The Pathway-2 study revealed that similar reductions in vascular resistance after spironolactone and doxazosin resulted in opposite effects on sodium balance, water retention, and hemodynamic parameters. These and other clinical findings were bridged to recent experimental and physiological data. Tissue sodium accumulation in salt-sensitive individuals due to endothelial glycocalyx dysfunction causes macrophage infiltration, vascular inflammation, and local changes in angiotensin-2 and aldosterone concentrations. This inflammatory cascade leads to factor XII-related coagulation disorders with neutrophil extracellular trap formation (NETosis). This model of sodium-induced microcirculation impairment was used to explain the differences in central hemodynamic parameters after spironolactone or doxazosin treatment in resistant hypertension. Hypertension treatment by induced sodium removal or reduced sodium intake should reduce endothelial glycocalyx dysfunction, inflammation, NETosis, and coagulation disorders, leading to improved vascular health and cardiac diastolic function.

中文翻译：

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钠引起的炎症——顽固性高血压的隐形参与者

本综述的目的是讨论钠和炎症在高血压病理生理学中的作用以及观察到的药物对不同血流动力学的影响。Pathway-2 研究表明，螺内酯和多沙唑嗪后血管阻力的类似降低对钠平衡、水潴留和血流动力学参数产生相反的影响。这些和其他临床发现与最近的实验和生理数据相联系。由于内皮糖萼功能障碍，盐敏感个体的组织钠积累会导致巨噬细胞浸润、血管炎症以及血管紧张素 2 和醛固酮浓度的局部变化。这种炎症级联反应导致与中性粒细胞胞外陷阱形成 (NETosis) 的因子 XII 相关的凝血障碍。这种钠诱导的微循环障碍模型用于解释顽固性高血压患者在螺内酯或多沙唑嗪治疗后中心血流动力学参数的差异。通过诱导钠去除或减少钠摄入量治疗高血压应减少内皮糖萼功能障碍、炎症、NETosis 和凝血障碍，从而改善血管健康和心脏舒张功能。