Tempol Alters Urinary Extracellular Vesicle Lipid Content and Release While Reducing Blood Pressure during the Development of Salt-Sensitive Hypertension.
Tempol Alters Urinary Extracellular Vesicle Lipid Content and Release While Reducing Blood Pressure during the Development of Salt-Sensitive Hypertension.
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DOI：
10.3390/biom11121804
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发表时间：
2021-12-01
期刊：
影响因子：
5.5
通讯作者：
Alli AA
中科院分区：
文献类型：
--
作者：
Chacko KM;Nouri MZ;Schramm WC;Malik Z;Liu LP;Denslow ND;Alli AA
高盐摄入后血压升高导致的盐敏感性高血压与活性氧（ROS）产生的增加有关。众所周知，ROS 会增加上皮钠通道 (ENaC) 的活性，因此，它们对钠潴留和血压升高有间接影响。细胞外囊泡 (EV) 携带各种分子，包括蛋白质、微小 RNA 和脂质，在健康和疾病中的细胞间通讯和细胞内信号传导中发挥作用。我们研究了盐敏感性高血压 129Sv 小鼠服用抗氧化剂 Tempol 后 EV 脂质、尿电解质、渗透压、血压以及肾 ENaC 及其衔接蛋白 MARCKS/MARCKS 样蛋白 1 (MLP1) 表达的变化。我们的结果显示，Tempol 输注可降低高血压 129Sv 小鼠肾皮质中的收缩压以及 ENaC 和 MARCKS α 亚基的蛋白质表达。我们的脂质组学数据显示，经过 Tempol 治疗后，这些小鼠的尿液 EV 中二酰基甘油和单酰基甘油含量增加，神经酰胺、二氢神经酰胺和三酰基甘油含量减少。这些数据将使我们深入了解涉及旨在抑制 ROS 以缓解盐敏感性高血压的策略的机制。
Salt-sensitive hypertension resulting from an increase in blood pressure after high dietary salt intake is associated with an increase in the production of reactive oxygen species (ROS). ROS are known to increase the activity of the epithelial sodium channel (ENaC), and therefore, they have an indirect effect on sodium retention and increasing blood pressure. Extracellular vesicles (EVs) carry various molecules including proteins, microRNAs, and lipids and play a role in intercellular communication and intracellular signaling in health and disease. We investigated changes in EV lipids, urinary electrolytes, osmolality, blood pressure, and expression of renal ENaC and its adaptor protein, MARCKS/MARCKS Like Protein 1 (MLP1) after administration of the antioxidant Tempol in salt-sensitive hypertensive 129Sv mice. Our results show Tempol infusion reduces systolic blood pressure and protein expression of the alpha subunit of ENaC and MARCKS in the kidney cortex of hypertensive 129Sv mice. Our lipidomic data show an enrichment of diacylglycerols and monoacylglycerols and reduction in ceramides, dihydroceramides, and triacylglycerols in urinary EVs from these mice after Tempol treatment. These data will provide insight into our understanding of mechanisms involving strategies aimed to inhibit ROS to alleviate salt-sensitive hypertension.
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