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Endocrine Abstracts (2012) 29 S48.3

1University of Regensburg, Regensburg, Germany; 2INSERM, Paris Cardiovascular Research Center, Paris, France; 3AOU S.Giovanni Battista, Torino, Italy; 4Klinikum der Universität München, München, Germany; 5CNRS, and Université de Nice Sophia Antipolis, Nice, France.


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, Lifton and co-workers have described somatic mutations of the K+ channel KCNJ5 in aldosterone producing adenoma. Recent follow-up studies have confirmed the concept that pore-region mutations turn KCNJ5 into a Na+-permeable channel. Interestingly, such mutations can be found in more than 30% of aldosterone producing adenomas.

For TASK1 and TASK3, no human phenotype has been described so far. However, knockout mice for TASK1 and TASK3 have highlighted the functional relevance of these channels: Before puberty, inactivation of the TASK1 gene resulted in autonomous aldosterone production and caused an aberrant expression of aldosterone synthase in zona fasciculata cells that normally produce only glucocorticoids. After puberty, male mice were able to compensate for the defect of TASK1 and their aldosterone synthase regained regular localization in glomerulosa cells. In female TASK1 knockout mice, dyszonation of the aldosterone synthase and hyperaldosteronism persisted after puberty.

In TASK3 knockout mice, plasma renin activity was suppressed and the aldosterone/renin ratio, an indicator of autonomous aldosterone production, was elevated. TASK3 knockout animals were unable to adapt aldosterone production to dietary salt intake in a normal way. The inappropriately high aldosterone levels under high dietary salt resulted in arterial hypertension.

These novel data corroborate the concept that K+ channels play a critical role in adrenocortical cells. Dysfunction of adrenal K+ channels can lead to developmental deficits, hyperaldosteronism and adenoma formation and maladaptation of aldosterone secretion to dietary salt intake.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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