Gene-Sodium Interaction and Blood Pressure: Findings from Genomics Research of Blood Pressure Salt Sensitivity

被引:3
作者
Kelly, Tanika N. [1 ]
He, Jiang [1 ,2 ]
机构
[1] Tulane Univ, Sch Publ Hlth & Trop Med, Dept Epidemiol, New Orleans, LA 70118 USA
[2] Tulane Univ, Sch Med, Dept Med, New Orleans, LA 70112 USA
来源
RECENT ADVANCES IN NUTRIGENETICS AND NUTRIGENOMICS | 2012年 / 108卷
关键词
ANGIOTENSIN-ALDOSTERONE SYSTEM; ALPHA-ADDUCIN POLYMORPHISM; HYPERALDOSTERONISM TYPE-II; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2; CONGENITAL ADRENAL-HYPERPLASIA; CARDIOVASCULAR RISK-FACTORS; ATRIAL-NATRIURETIC-PEPTIDE; EPITHELIAL NA+ CHANNEL; LOW-RENIN HYPERTENSION; OXIDE SYNTHASE GENE;
D O I
10.1016/B978-0-12-398397-8.00010-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
High blood pressure (BP) is a complex trait determined by both genetic and environmental factors, as well as the interactions between these factors. Over the past few decades, there has been substantial progress in elucidating the genetic determinants underlying the BP response to sodium intake, or BP salt sensitivity. Research of monogenic BP disorders has highlighted the importance of renal salt handling in BP regulation, implicating genes and biological pathways related to salt sensitivity. Candidate gene studies have contributed important information toward understanding the genomic mechanisms underlying the BP response to salt intake, identifying genes in the renin-angiotensin-aldosterone system, renal sodium channels/transporters, and the endothelial system related to this phenotype. Despite these advancements, genome-wide association studies are still needed to uncover novel mechanisms underlying salt sensitivity, while future sequencing efforts promise the discovery of functional variants related to this complex trait. Delineating the genetic architecture of salt sensitivity will be critical to understanding how genes and dietary sodium interact to influence BP.
引用
收藏
页码:237 / 260
页数:24
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