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.
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Friedrich C. Luft (2000) studied this question.
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