The application of genetic strategies to studies of the pathogenesis of hypertension has proceeded on multiple fronts in the past year and has provided new insight into disease pathogenesis. Studies of monogenic forms of hypertension have led to the identification of genes causing Liddle's syndrome and the syndrome of apparent mineralocorticoid excess, while studies of essential hypertension have examined the potential roles of a number of candidate genes. Animal models have been exploited, both by mapping of naturally occurring mutations that alter blood pressure and by physiologic analysis of animals harboring specific engineered mutations.