| TASK1 and TASK3 potassium channels: determinants of aldosterone secretion and adrenocortical zonation. | |
| | |
MedLine Citation:
|
PMID: 20049674 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Potassium channels control the membrane voltage of aldosterone-producing zona glomerulosa cells. They are responsible for the unique K(+) sensitivity of these cells and are important molecular targets of angiotensin II signaling. Among the 78 pore-forming K(+) channels in human genome only a few are found in adrenal glands. The 2-P-domain K(+) channels TASK1 and TASK3 are strongly expressed in the adrenal cortex and produce a background K(+) conductance, which is pivotal for the regulation of the aldosterone secretion in zona glomerulosa cells. Disruption of the TASK1 gene in mice resulted in an autonomous aldosterone production and caused a remarkable aberrant expression of aldosterone synthase in zona fasciculata cells that normally produce glucocorticoids. After puberty, only in male mice aldosterone production was switched off in the zona fasciculata and regular zonation of aldosterone synthase occurred. In double mutant TASK1(-/-)/TASK3(-/-) mice, also adult male mice displayed primary hyperaldosteronism. Therefore, these knockout mice are interesting models to study mechanisms of autonomous aldosterone production and adrenocortical zonation. These data suggest that modifications of the adrenocortical K(+) conductances could also contribute to autonomic aldosterone production and primary hyperaldosteronism in humans. |
| | |
Authors:
|
S Bandulik; D Penton; J Barhanin; R Warth |
Related Documents
:
|
17640754 - Motor discoordination of transgenic mice overexpressing a microtubule destabilizer, sta... 7072984 - Defective thyroid ontogenesis in fetal hypothyroid (hyt/hyt) mice. 15579434 - Dysmorphogenesis of kidney cortical peritubular capillaries in angiopoietin-2-deficient... 11353514 - Variegated expression and delayed retinal pigmentation during development in transgenic... 12104094 - Cancerb increases production of nitric oxide and tumor necrosis factor-alpha in periton... 722074 - Beta-estradiol reduces natural killer cells in mice. |
Publication Detail:
|
Type: Journal Article; Review Date: 2010-01-04 |
Journal Detail:
|
Title: Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme Volume: 42 ISSN: 1439-4286 ISO Abbreviation: Horm. Metab. Res. Publication Date: 2010 Jun |
Date Detail:
|
Created Date: 2010-05-26 Completed Date: 2010-09-08 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 0177722 Medline TA: Horm Metab Res Country: Germany |
Other Details:
|
Languages: eng Pagination: 450-7 Citation Subset: IM |
Copyright Information:
|
Georg Thieme Verlag KG Stuttgart-New York. |
Affiliation:
|
Physiology, University of Regensburg, Regensburg, Germany. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adrenal Cortex
/
metabolism* Aldosterone / secretion* Animals Humans Mice Models, Biological Nerve Tissue Proteins / genetics, metabolism, physiology* Organ Specificity Potassium Channels / physiology Potassium Channels, Tandem Pore Domain / genetics, metabolism, physiology* Tissue Distribution |
| Chemical | |
Reg. No./Substance:
|
0/KCNK9 protein, human; 0/Nerve Tissue Proteins; 0/Potassium Channels; 0/Potassium Channels, Tandem Pore Domain; 0/potassium channel subfamily K member 3; 52-39-1/Aldosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Comorbidities in Primary Aldosteronism.
Next Document: Estradiol Supplementation Helps Overcome Central Leptin Resistance of Ovariectomized Mice on a High ...