Most researchers in genetics would agree that essential hypertension is one of the toughest multifactorial diseases to tackle. There are two main reasons for such difficulty. First, it is cumbegome to obtain reliable measurements of the target phenotype, blood pressure (BP). BP shows much quicker and larger fluctuations than do other pheno-types (for example, blood glucose level). Second, after many genetic studies, we have realized that genomic variations making up the genetic susceptibility to hypertension seem to be much broader than previously expected. Even worse, single genetic variations have very small effects and may have complex interactions with other genes and environments. This has been suggested in both rats and humans. Results of large-scale genome-wide association studies (GWASs) recently published indicate that the association of each single nucleotide polymorphism (SNP) with hypertension is quite weak. Indeed, it may require a huge number of SNPs to explain the total genetic variance of BP, if the effects of such SNPs are assumed to be additive.
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