Linked Life Data

21111026

Source:http://linkedlifedata.com/resource/pubmed/id/21111026

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2011-3-7
pubmed:abstractText
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 NH(4)Cl 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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1872-8057
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
336
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
47-52
pubmed:dateRevised
2011-11-7
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
TASK channels are not required to mount an aldosterone secretory response to metabolic acidosis in mice.
pubmed:affiliation
University of Virginia, Department of Pharmacology, 1340 Jefferson Park Ave., Charlottesville, VA 22908, USA. Nag4g@virginia.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural