Searchable abstracts of presentations at key conferences in endocrinology

ea0029s48.3 | Pathogenesis of primary aldosteronism | ICEECE2012

Potassium channels in primary aldosteronism

Warth R. , Bandulik S. , Penton D. , Tauber P. , Zennaro M. , Mulatero P. , Beuschlein F. , Barhanin J.

Potassium channels regulate the membrane voltage of aldosterone-producing glomerulosa cells in the adrenal glands. They are required for the unique K+ sensitivity of these cells and are targets of angiotensin II signaling. Several K+ channels show high levels of expression in the adrenal cortex and are believed to be important for the control of hormone secretion, e.g. KCNJ5, TASK1, TASK3, KCNMA1, and KCNQ1.In a pioneering study, Li...

ea0029oc13.2 | Adrenal Basic | ICEECE2012

VSNL1 is upregulated in aldosterone producing adenomas with KCNJ5 mutations and protects from calcium-induced apoptosis

Monticone S. , Crudo V. , Burrello J. , Galmozzi M. , Warth R. , Veglio F. , Mulatero P. , Williams T.

Visinin-like 1 (VSNL1) is upregulated in aldosterone-producing adenomas (APA) compared to normal adrenals. We demonstrate that VSNL1 overexpression in adrenocortical carcinoma cells (NCI H295R) upregulates basal and angiotensin II (Ang II)-stimulated CYP11B2 gene expression 3.2- and 1.5-fold, respectively. Conversely, silencing VSNL1 by RNA interference decreases Ang II-stimulated CYP11B2 expression and aldosterone secretion by 41 and 34.5%, respectively. Mutations in the pota...

ea0029p37 | Adrenal cortex | ICEECE2012

Deletion of TASK3 K+ channels leads to hyperaldosteronism in neonatal mice

Bandulik S. , Tauber P. , Penton-Ribas D. , Tegtmeier I. , Lesage F. , Barhanin J. , Warth R.

Depolarisation of adrenal zona glomerulosa cells is a pivotal event for the secretion of aldosterone. Potassium channels like TASK1 and TASK3 are highly expressed in the adrenal cortex and determine the membrane voltage. Deletion of TASK3 K+ channels in mice caused a severe age-dependent hyperaldosteronism. The aim of this study was to identify the mechanisms underlying this phenotype.Neonatal TASK3-/- mice (ko) showed higher plasma aldosteron...

ea0029p32 | Adrenal cortex | ICEECE2012

KCNJ5 Mutations in European Families with Non-Glucocorticoid Remediable Familial Hyperaldosteronism

Mulatero P. , Tauber P. , Zennaro M. , Monticone S. , Lang K. , Beuschlein F. , Fischer E. , Burrello J. , Pallauf A. , Galmozzi M. , Amar L. , Williams T. , Strom T. , Graf E. , Bandulik S. , Penton D. , Plouin P. , Warth R. , Allolio B. , Jeunemaitre X. , Veglio F. , Reincke M.

Primary Aldosteronism (PA) is the most frequent cause of endocrine hypertension. Three forms of familial hyperaldosteronism (FH) have been described, named FH-I to -III. Recently, a mutation of KCNJ5 has been shown to be associated with FH-III, whereas the cause of FH-II is still unknown. In this study we searched for mutations in KCNJ5 in 46 patients from 21 families with FH, in which FH-I was excluded. We identified a new germline G151E mutation in two PA affected subjects f...