Strazzullo Pasquale, Galletti Ferruccio
Department of Clinical and Experimental Medicine, Federico II University of Naples Medical School, Via S. Pansini, 5, 80131 Naples, Italy.
Curr Hypertens Rep. 2007 Mar;9(1):25-32. doi: 10.1007/s11906-007-0006-6.
Excess dietary salt intake represents a predominant cause of hypertension. However, individual blood pressure response to salt is heterogeneous, possibly due to different inherited susceptibility. The early identification of rare monogenic forms of hypertension associated with abnormalities of renal tubular sodium handling and response to diuretics highlighted the important role of renal alterations in salt-sensitive hypertension. Thereafter, interest has concentrated on the identification of more common allelic variants of candidate genes for hypertension in relation to the salt-sensitivity phenotype. By now, relatively large numbers of such variants have been described, and the pathogenic role of gene-gene interaction has received increasing attention. The alternative approach, consisting of the search for quantitative trait loci in the human genome linked to the transmission of salt-sensitive hypertension, has so far been less successful and cost-effective. This review summarizes consolidated knowledge and discusses the most recent novel findings on the impact of genetic variance on salt-sensitivity of blood pressure.
过量摄入膳食盐是高血压的主要成因。然而,个体对盐的血压反应存在异质性,这可能是由于不同的遗传易感性所致。早期发现与肾小管钠处理异常及对利尿剂反应相关的罕见单基因高血压形式,凸显了肾脏改变在盐敏感性高血压中的重要作用。此后,研究兴趣集中在确定与盐敏感性表型相关的高血压候选基因中更常见的等位基因变体。到目前为止,已经描述了相对大量的此类变体,并且基因-基因相互作用的致病作用受到了越来越多的关注。另一种方法是在人类基因组中寻找与盐敏感性高血压传递相关的数量性状位点,但迄今为止,这种方法的成功率和成本效益较低。这篇综述总结了已有的知识,并讨论了关于基因变异对血压盐敏感性影响的最新研究发现。