For HT there were no SNPs with significance below 5×10-7 (Table 3) but the number and distribution of association signals in the range 10-4 to 10-7 was similar to that of the other diseases studied (Table 4 and Supplementary Table 7). There are several possible explanations. First, HT may have fewer common risk alleles of larger effect sizes than some of the other complex phenotypes. If so, then identification of susceptibility variants for HT is likely be reliant on the synthesis of findings from multiple large-scale studies. Second, the present study may have failed to detect genuine common susceptibility variants of large effect size they happened to be poorly tagged by the set of SNPs genotyped in the current study. If so, further rounds of genotyping using resources that offer increased density (or complementary SNP sets), and/or improved analytical methods (for example, imputation-based) should facilitate their discovery. Third, study of HT may be more susceptible than other phenotypes to the diluting effects of misclassification bias due to the presence of hypertensive individuals within the control samples. If so, power can be improved in future studies by use of controls specifically screened to exclude individuals with elevated blood pressure.
