Genetic approach to diagnostic and therapeutic decisions in human hypertension.
In the most exciting genetic advances in the diagnosis of essential hypertension, genes responsible for three distinct forms of low-renin hypertension have been identified. Two of these forms are dominant: glucocorticoid remediable hypertension (a new gene created by the fusion of the 11 beta-hydroxylase and aldosterone synthase genes) and Liddle's syndrome (a defect in the epithelial sodium channel). One of the forms is recessive: the syndrome of apparent mineralocorticoid excess (a defect in renal 11 beta-hydroxysteroid dehydrogenase). The role of more than 20 other genes in causing hypertension has been assessed with variable findings. The most convincing evidence supports a role for the angiotensinogen gene, where linkage has been documented and an association with an intermediate phenotype of hypertension (nonmodulation) has been reported.
Williams
G H
GH
Endocrine-Hypertension Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
Fisher
N D
ND
D000808:Angiotensinogen / Q000235:genetics; D000818:Animals; D008040:Genetic Linkage; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000235:genetics* / Q000628:therapy; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D010641:Phenotype; D012084:Renin-Angiotensin System / Q000235:genetics*; D013577:Syndrome
D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A