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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...

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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...

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Endocrine Abstracts

Potassium channels in primary aldosteronism

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

BiosciAbstracts

Endocrine Abstracts

Potassium channels in primary aldosteronism

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

BiosciAbstracts

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