High-salt intake increases TRPC3 expression and enhances TRPC3-mediated calcium influx and systolic blood pressure in hypertensive patients
High-salt intake increases TRPC3 expression and enhances TRPC3-mediated calcium influx and systolic blood pressure in hypertensive patients
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高盐摄入会增加高血压患者中 TRPC3 的表达并增强 TRPC3 介导的钙内流和收缩压
DOI：
10.1038/s41440-020-0409-1
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发表时间：
2020
影响因子：
5.4
通讯作者：
Li Zhiyong
中科院分区：
文献类型：
--
作者：
Hu Yingru;Xia Weijie;Li Yingsha;Wang Qianran;Lin Shaoyang;Wang Bin;Zhou Cui;Cui Yuanting;Jiang Yanli;Pu Xiaona;Wei Xiao;Wu Hao;Zhang Hengshu;Zhu Zhiming;Liu Daoyan;Li Zhiyong
高血压大鼠和患者单核细胞瞬时受体电位典型亚型3（TRPC 3）表达增强和TRPC 3介导的钙内流与血压升高相关。每日盐摄入量与高血压密切相关，但TRPC 3表达与盐摄入量之间的关系尚未在高血压患者中进行评估。采用逆转录-聚合酶链反应，我们研究了高血压和正常血压对照组外周血单个核细胞（PBMCs）中TRPC 3和TRPC 3相关钙库操纵的钙内流（SOCE）的表达。使用荧光染料Fura-2 AM进行SOCE的测量。根据24小时尿钠排泄量将参与者分为低盐组（<9 g）和高盐组（≥9 g）。THP-1细胞经高浓度NaCl处理后TRPC 3 mRNA表达水平和SOCE增加。然而，TRPC 3特异性抑制剂Pyr 3的施用显著降低了该效果。此外，TRPC 3 mRNA表达水平从高盐摄入量的原发性高血压患者的PBMC中显着高于低盐摄入量的患者与血压正常的对照组相比。我们还观察到高血压受试者（而不是血压正常的对照受试者）的PBMC中TRPC 3介导的SOCE显著增加，钙浓度与盐摄入量相关。更重要的是，TRPC 3 mRNA水平与原发性高血压患者的盐摄入量和收缩压显著相关。这项研究首次证明，TRPC 3 mRNA水平的增加与高血压患者的盐摄入量和收缩压升高有关。
Enhanced transient receptor potential canonical subtype 3 (TRPC3) expression and TRPC3-mediated calcium influx in monocytes from hypertensive rats and patients are associated with increased blood pressure. Daily salt intake is closely related to hypertension, but the relationship between TRPC3 expression and salt intake has not yet been evaluated in hypertensive patients. Using reverse transcription-polymerase chain reaction, we studied the expression of TRPC3 and TRPC3-related store-operated calcium entry (SOCE) in peripheral blood mononuclear cells (PBMCs) from hypertensive and normotensive control subjects. Measurement of SOCE was performed using the fluorescent dye Fura-2 AM. Participants were divided into a low-salt group (<9 g) and a high-salt group (≥9 g) based on 24-h urinary sodium excretion. Increased TRPC3 mRNA expression levels and SOCE were observed in THP-1 cells after high-NaCl treatment. However, administration of the TRPC3-specific inhibitor Pyr3 significantly decreased the effect. Furthermore, the TRPC3 mRNA expression levels in PBMCs from high-salt intake patients with essential hypertension were significantly higher than those in low-salt intake patients compared with those in normotensive control subjects. We also observed significantly increased TRPC3-mediated SOCE in PBMCs from hypertensive subjects (but not from normotensive control subjects), with calcium concentration correlating with salt intake. More importantly, TRPC3 mRNA levels showed a significant correlation with salt intake and systolic blood pressure in patients with essential hypertension. This study demonstrated, for the first time, that increased TRPC3 mRNA levels are associated with elevated salt intake and systolic blood pressure in hypertensive patients.