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Genomics and pharmacogenomics of salt-sensitive hypertension

机译:盐敏感性高血压的基因组学和药物基因组学

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Salt sensitivity is estimated to be present in 51% of the hypertensive and 26% of the normotensive populations. The individual blood pressure response to salt is heterogeneous and possibly related to inherited susceptibility. Although the mechanisms underlying salt sensitivity are complex and not well understood, genetics can help to determine the blood response to salt intake. So far only a few genes have been found to be associated with salt-sensitive hypertension using candidate gene association studies. The kidney is critical to overall fluid and electrolyte balance and long-term regulation of blood pressure. Thus, the pathogenesis of salt sensitivity must involve a derangement in renal NaCl handling: an inability to decrease renal sodium transport and increase sodium excretion in the face of an increase in NaCl load that could be caused by aberrant counter-regulatory natriuretic/antinatriuretic pathways. We review here the literature regarding the gene variants associated with salt-sensitive hypertension and how the presence of these gene variants influences the response to antihypertensive therapy.
机译:盐敏感性估计存在于51%的高血压人群和26%的正常血压人群中。个体对盐的血压反应是异质的,可能与遗传易感性有关。尽管对盐敏感性的潜在机制很复杂并且尚未得到很好的理解,但是遗传学可以帮助确定血液对盐摄入的反应。到目前为止,使用候选基因关联研究发现只有少数基因与盐敏感性高血压有关。肾脏对于整体液体和电解质平衡以及长期调节血压至关重要。因此,盐敏感性的发病机制必须涉及肾脏NaCl处理的失调:面对异常的反调节利尿钠/利尿钠通路可能导致的NaCl负荷增加,无法降低肾脏钠转运和增加钠排泄。我们在这里复习与盐敏感性高血压相关的基因变体以及这些基因变体的存在如何影响对降压治疗的反应的文献。

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