BACKGROUND:Every year, thousands of patients with hypertension reduce salt consumption in the efforts to control their blood pressure. However, hypertension has a self-sustaining character in a significant part of the population. We hypothesized that chronic hypertension leads to irreversible renal damage that remains after removing the trigger, causing an elevation of the initial blood pressure.METHODS:Dahl salt-sensitive rat model was used for chronic, continuous observation of blood pressure. Rats were fed a high salt diet to induce hypertension, and then the diet was switched back to normal sodium content.RESULTS:We found that developed hypertension was irreversible by salt cessation: after a short period of reduction, blood pressure grew even higher than in the high-salt phase. Notably, the self-sustaining phase of hypertension was sensitive to benzamil treatment due to sustaining epithelial sodium channel hyperactivity, as shown with patch-clamp analysis. Glomerular damage and proteinuria were also irreversible. In contrast, some mechanisms, contributing to the development of salt-sensitive hypertension, normalized after salt restriction. Thus, flow cytometry demonstrated that dietary salt reduction in hypertensive animals decreased the number of total CD45⁺, CD3⁺CD4⁺, and CD3⁺CD8⁺ cells in renal tissues. Also, we found tubular recovery and improvement of glomerular filtration rate in the postsalt period versus a high-salt diet.CONCLUSIONS:Based on earlier publications and current data, poor response to salt restriction is due to the differential contribution of the factors recognized in the developmental phase of hypertension. We suggest that proteinuria or electrolyte transport can be prioritized over therapeutic targets of inflammatory response.

中文翻译：

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Dahl 大鼠停止高盐饮食后高血压与肾损伤的分离

背景：每年，成千上万的高血压患者为了控制血压而减少盐的摄入量。然而，高血压在很大一部分人群中具有自我维持的特征。我们推测，慢性高血压会导致不可逆的肾损伤，在去除触发因素后，肾损伤仍然存在，导致初始血压升高。方法：采用Dahl盐敏感大鼠模型进行长期、连续的血压观察。给大鼠喂食高盐饮食以诱发高血压，然后将饮食转回正常钠含量。结果：我们发现，戒盐后发生的高血压是不可逆转的：在短期减少盐摄入后，血压甚至比之前更高。高盐阶段。值得注意的是，如膜片钳分析所示，由于维持上皮钠通道过度活跃，高血压的自我维持阶段对苯扎米尔治疗敏感。肾小球损伤和蛋白尿也是不可逆的。相反，一些导致盐敏感性高血压发生的机制在限盐后恢复正常。因此，流式细胞术表明，高血压动物饮食中盐的减少减少了肾组织中CD45 ⁺、CD3 ⁺ CD4 ⁺和CD3 ⁺ CD8 ⁺细胞的总数。此外，我们发现与高盐饮食相比，盐后时期肾小管恢复和肾小球滤过率改善。结论：根据早期出版物和当前数据，对盐限制的反应不佳是由于在盐饮食中认识到的因素的不同贡献所致。高血压的发展阶段。我们建议蛋白尿或电解质转运可以优先于炎症反应的治疗目标。