Journal
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY
Volume 467, Issue 5, Pages 1027-1042Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00424-014-1628-6
Keywords
KCNK2; KCNK3; KCNK9; TASK; TREK; Aldosterone
Categories
Funding
- Deutsche Forschungsgemeinschaft [FOR1086]
- French Agence Nationale pour la Recherche (ANR) BeyondTASKs grant
- LabEx Ion Channel Science and Therapeutics grant [ANR-11-LABX-0015-01]
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The physiological control of steroid hormone secretion from the adrenal cortex depends on the function of potassium channels. The two-pore domain K+ channels (K2P) TWIK-related acid sensitive K+ channel 1 (TASK1), TASK3, and TWIK-related K+ channel 1 (TREK1) are strongly expressed in adrenocortical cells. They confer a background K+ conductance to these cells which is important for the K+ sensitivity as well as for angiotensin II and adrenocorticotropic hormone-dependent stimulation of aldosterone and cortisol synthesis. Mice with single deletions of the Task1 or Task3 gene as well as Task1/Task3 double knockout mice display partially autonomous aldosterone synthesis. It appears that TASK1 and TASK3 serve different functions: TASK1 affects cell differentiation and prevents expression of aldosterone synthase in the zona fasciculata, while TASK3 controls aldosterone secretion in glomerulosa cells. TREK1 is involved in the regulation of cortisol secretion in fasciculata cells. These data suggest that a disturbed function of K2P channels could contribute to adrenocortical pathologies in humans.
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