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Primary aldosteronism is a disorder characterized by hypertension and, in more severe form, hypokalemia, due to autonomous aldosterone secretion from the adrenocortical zona glomerulosa. Improved screening techniques, particularly application of the plasma aldosterone: plasma renin activity ratio, has led to renewed interest in Conn's original proposal that primary aldosteronism may be the cause of increased blood pressure in about 10% of adults with hypertension. Glucocorticoid\u2010remediable aldosteronism (GRA) was the first described familial form of hyperaldosteronism. The disorder is characterized by aldosterone secretory function regulated chronically by ACTH. Hence, aldosterone hypersecretion can be chronically suppressed by exogenous glucocorticoids such as dexamethasone in physiologic\u2010range doses. This autosomal dominant disorder has been shown to be caused by a hybrid gene mutation formed by a cross\u2010over of genetic material between the ACTH\u2010responsive regulatory portion of the 11b\u2010hydroxylase (CYP11B1) gene and the coding region of the aldosterone synthase (CYP11B2) gene. Familial hyperaldosteronism type II (FH\u2010II), so named to distinguish the disorder from GRA or familial hyperaldosteronism type I (FH\u2010I), is characterized by inheritance consistent with an autosomal dominant pattern of autonomous aldosterone hypersecretion which is not suppressible by dexamethasone. Linkage analysis in a single large kindred, and direct mutation screening, has shown that this disorder is unrelated to mutations in the genes for aldosterone synthase or the angiotensin II receptor. A recent genome\u2010wide search has identified a genetic linkage between FH\u2010II in this single large kindred and polymorphic gene markers on chromosome 7 in a region that corresponds to cytogenetic band 7p22. This is the first identified locus for FH\u2010II. Several possible candidate genes have been localized to the 7p22 region. The precise genetic cause of FH\u2010II remains to be elucidated.<\/jats:p>","DOI":"10.1111\/j.1749-6632.2002.tb04414.x","type":"journal-article","created":{"date-parts":[[2009,7,9]],"date-time":"2009-07-09T18:38:20Z","timestamp":1247164700000},"page":"77-88","source":"Crossref","is-referenced-by-count":47,"title":["New Genetic Insights in Familial Hyperaldosteronism"],"prefix":"10.1111","volume":"970","author":[{"given":"RICHARD V.","family":"JACKSON","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ANTHONY","family":"LAFFERTY","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"DAVID J.","family":"TORPY","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"CONSTANTINE","family":"STRATAKIS","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2006,1,24]]},"reference":[{"key":"e_1_2_7_2_2","doi-asserted-by":"crossref","first-page":"20961","DOI":"10.1016\/S0021-9258(19)30030-4","article-title":"Characterisation of the two genes encoding human steroid 11\u03b2\u2010hydroxylase (P\u2010450 (11)\u03b2)","volume":"264","author":"Mornet E.","year":"1989","journal-title":"J. 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