A genetic influence on the variability of blood pressure in populations has been established. This effect has been demonstrated repeatedly by the presence of familial aggregation of blood pressure; however, a unique bimodal distribution in populations has not been established. About one-third to one-half of the blood pressure variance is explained by heredity with the remainder due to environmental or unknown factors. Direct associations of blood pressure with genetic markers in populations have been described infrequently. However, an association between haptoglobin 1 and increased blood pressure has been reported. This relationship is possibly secondary to increased sodium sensitivity in this genetic subgroup. The familial aggregation of urinary kallikrein as well as sodium-lithium countertransport and hypertension represents a successful attempt by investigators to identify correlates of intermediate phenotypes of hypertension. The association between restriction fragment length polymorphisms and elevated blood pressure represents an unmet potential. It should be emphasized that any genetic predictive factor will be affected by environmental factors. This interaction provides the opportunity for possible modification or prevention of hypertension by hygienic means.