The year 1999 saw considerable activity in the area of hypertension-related molecular genetics. Several new monogenic hypertensive disorders, as well as a monogenic form of hypotension, were elucidated. Molecular genetics has made significant inroads in explaining basic mechanisms of magnesium homeostasis, Linkage strategies have been applied in family studies, sib-pair analyses, and twin studies. More stringent criteria for association studies have been formulated. The 11 beta-hydroxysteroid dehydrogenase gene, the prostacyclin synthase gene, genes coding for variants in G proteins, and adrenergic receptor genes have received particular attention. On the horizon are better phenotyped patient and subject collectives, expanded genotyping with the availability of a 300 000 genome-wide single-nucleotide polymorphism map, multigenic studies in the form of metabolic control analyses, and new bioinformatic strategies including neural networks. Curr Opin Nephrol Hypertens 9:259-266. (C) 2000 Lippincott Williams & Wilkins.