Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 336, Issue 1-2, Pages 47-52Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2010.11.017
Keywords
Metabolic acidosis; Aldosterone; Renin; TASK; Angiotensin II; Zona glomerulosa
Categories
Funding
- NHLBI NIH HHS [R01 HL036977, R01 HL089717, R01 HL089717-03] Funding Source: Medline
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The stimulation of aldosterone production by acidosis enhances proton excretion and serves to limit disturbances in systemic acid-base equilibrium. Yet, the mechanisms by which protons stimulate aldosterone production from cells of the adrenal cortex remain largely unknown. TWIK-related acid sensitive K channels (TASK) are inhibited by extracellular protons within the physiological range and have emerged as important regulators of aldosterone production in the adrenal cortex. Here we show that congenic C57BL/6J mice with genetic deletion of TASK-1 (K(2P)3.1) and TASK-3 (K(2P)9.1) channel subunits overproduce aldosterone and display an enhanced sensitivity to steroidogenic stimuli, including a more pronounced steroidogenic response to chronic NH4Cl loading. Thus, we conclude that TASK channels are not required for the stimulation of aldosterone production by protons but their inhibition by physiological acidosis may contribute to full expression of the steroidogenic response. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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