Vascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.
Department of Nutrition and Integrative Physiology, Florida State University, Tallahassee, Florida, United States.
Am J Physiol Heart Circ Physiol. 2024 Oct 1;327(4):H896-H907. doi: 10.1152/ajpheart.00242.2024. Epub 2024 Aug 16.
Excess sodium consumption contributes to arterial dysfunction in humans. The C57BL/6 strain of mice has been used to identify mechanisms by which arterial dysfunction occurs after excess sodium consumption. However, there are concerns that C57BL/6 mice have strain-specific resistance to high-sodium (HS) diet-induced hypertension. To address this concern, we performed a meta-analysis to determine if excess sodium consumption in C57BL/6 mice induces arterial dysfunction. Databases were searched for HS versus standard diet studies that measured arterial function [i.e., systolic blood pressure (BP), endothelium-dependent dilation (EDD), and central arterial stiffness] in C57BL/6 mice. A total of 39 studies were included, demonstrating that the HS condition resulted in higher systolic BP than control mice with a mean difference of 9.8 mmHg (95% confidence interval [CI] = [5.6, 14], < 0.001). Subgroup analysis indicated that the systolic BP was higher in HS compared with the control condition when measured during night compared with daytime with telemetry ( < 0.001). We also identified that the difference in systolic BP between HS and control was ∼2.5-fold higher when administered through drinking water than through food ( < 0.001). A total of 12 studies were included, demonstrating that the HS condition resulted in lower EDD than control with a weighted mean difference of -12.0% (95% CI = [-20.0, -4.1], = 0.003). It should be noted that there was considerable variability across studies with more than half of the studies showing no effect of the HS condition on systolic BP or EDD. In summary, excess sodium consumption elevates systolic BP and impairs EDD in C57BL/6 mice. C57BL/6 mice are perceived as resistant to high-sodium diet-induced arterial dysfunction. This meta-analysis demonstrates that excess sodium consumption elevates blood pressure and impairs endothelium-dependent dilation in C57BL/6 mice. Nighttime measurements show more pronounced blood pressure elevation. In addition, sodium administration via drinking water, compared with food, induces a greater blood pressure elevation. These findings may be influenced by outlier studies, as the majority of studies showed no adverse effect of excess sodium consumption on arterial function.
过量摄入钠会导致人类动脉功能障碍。C57BL/6 品系的小鼠已被用于鉴定过量摄入钠后动脉功能障碍发生的机制。然而，人们担心 C57BL/6 小鼠对高钠（HS）饮食诱导的高血压具有特定的抗性。为了解决这一担忧，我们进行了一项荟萃分析，以确定 C57BL/6 小鼠过量摄入钠是否会导致动脉功能障碍。我们在数据库中搜索了 HS 与标准饮食研究，这些研究测量了 C57BL/6 小鼠的动脉功能[即收缩压（BP）、内皮依赖性扩张（EDD）和中央动脉僵硬]。共纳入 39 项研究，结果表明 HS 组的收缩压明显高于对照组，平均差异为 9.8mmHg（95%置信区间[CI]：[5.6，14]， < 0.001）。亚组分析表明，与白天相比，HS 组夜间的收缩压更高（通过遥测），差异有统计学意义（ < 0.001）。我们还发现，通过饮水给予 HS 组与通过食物给予 HS 组相比，HS 组与对照组之间的收缩压差异高 2.5 倍（ < 0.001）。共纳入 12 项研究，结果表明 HS 组的 EDD 明显低于对照组，加权平均差异为-12.0%（95%CI：[-20.0，-4.1]， = 0.003）。需要注意的是，大多数研究未显示 HS 组对收缩压或 EDD 有影响，因此各研究间存在较大的变异性。总之，过量摄入钠可使 C57BL/6 小鼠的收缩压升高，并损害其内皮依赖性扩张功能。C57BL/6 小鼠被认为对高钠饮食诱导的动脉功能障碍具有抗性。本荟萃分析表明，过量摄入钠可使 C57BL/6 小鼠的血压升高并损害其内皮依赖性扩张功能。夜间测量显示血压升高更为明显。此外，与食物相比，通过饮水给予钠可引起更大的血压升高。这些发现可能受到离群值研究的影响，因为大多数研究显示过量摄入钠对动脉功能没有不良影响。
