Division of Health Science Research, Fukushima Welfare Federation of Agricultural Cooperatives, Fukushima, Japan.
Curr Hypertens Rep. 2011 Feb;13(1):55-66. doi: 10.1007/s11906-010-0167-6.
The assessment of salt sensitivity of blood pressure is difficult because of the lack of universal consensus on definition. Regardless of the variability in the definition of salt sensitivity, increased salt intake, independent of the actual level of blood pressure, is also a risk factor for cardiovascular morbidity and mortality and kidney disease. A modest reduction in salt intake results in an immediate decrease in blood pressure, with long-term beneficial consequences. However, some have suggested that dietary sodium restriction may not be beneficial to everyone. Thus, there is a need to distinguish salt-sensitive from salt-resistant individuals, but it has been difficult to do so with phenotypic studies. Therefore, there is a need to determine the genes that are involved in salt sensitivity. This review focuses on genes associated with salt sensitivity, with emphasis on the variants associated with salt sensitivity in humans that are not due to monogenic causes. Special emphasis is given to gene variants associated with salt sensitivity whose protein products interfere with cell function and increase blood pressure in transgenic mice.
血压盐敏感性评估较为困难,因为其定义尚未达成共识。无论盐敏感性的定义存在何种差异,增加盐的摄入(与实际血压水平无关)也是心血管发病率和死亡率及肾脏疾病的一个风险因素。适度减少盐的摄入可即刻降低血压,并带来长期的益处。然而,有人认为,膳食钠限制可能并非对所有人都有益。因此,需要区分盐敏感者和盐抵抗者,但表型研究很难做到这一点。因此,需要确定与盐敏感性相关的基因。本综述重点关注与盐敏感性相关的基因,特别强调与人类盐敏感性相关的、非单基因病因所致的变异。特别关注与盐敏感性相关的基因变异,这些变异的蛋白产物会干扰细胞功能,并使转基因小鼠的血压升高。