Source:http://linkedlifedata.com/resource/pubmed/id/17579662
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
2007-8-23
|
pubmed:abstractText |
The kidney is the major regulator of potassium homeostasis. In addition to the ROMK channels, large conductance Ca(2+)-activated K(+) (BK) channels are expressed in the apical membrane of the aldosterone sensitive distal nephron where they could contribute to renal K(+) secretion. We studied flow-induced K(+) secretion in BK channel alpha-subunit knockout (BK(-/-)) mice by acute pharmacologic blockade of vasopressin V(2) receptors, which caused similar diuresis in wild-type and knockout mice. However, wild-type mice, unlike the BK(-/-), had a concomitant increase in urinary K(+) excretion and a significant correlation between urinary flow rate and K(+) excretion. Both genotypes excreted similar urinary amounts of K(+) irrespective of K(+) diet. This was associated, however, with higher plasma aldosterone and stronger expression of ROMK in the apical membrane of the aldosterone-sensitive portions of the distal nephron in the knockout than in the wild-type under control diet and even more so with the high-K(+) diet. High-K(+) intake significantly increased the renal expression of the BK channel in the wild-type mouse. Finally, despite the higher plasma K(+) and aldosterone levels, BK(-/-) mice restrict urinary K(+) excretion when placed on a low-K(+) diet to the same extent as the wild-type. These studies suggest a role of the BK channel alpha-subunit in flow-induced K(+) secretion and in K(+) homeostasis. Higher aldosterone and an upregulation of ROMK may compensate for the absence of functional BK channels.
|
pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Kcnj1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Large-Conductance...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Inwardly...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vasopressin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
0085-2538
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
72
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
566-73
|
pubmed:dateRevised |
2010-12-3
|
pubmed:meshHeading |
pubmed-meshheading:17579662-Animals,
pubmed-meshheading:17579662-Gene Expression Regulation,
pubmed-meshheading:17579662-Genotype,
pubmed-meshheading:17579662-Homeostasis,
pubmed-meshheading:17579662-Kidney,
pubmed-meshheading:17579662-Large-Conductance Calcium-Activated Potassium Channels,
pubmed-meshheading:17579662-Mice,
pubmed-meshheading:17579662-Mice, Knockout,
pubmed-meshheading:17579662-Potassium,
pubmed-meshheading:17579662-Potassium Channels, Inwardly Rectifying,
pubmed-meshheading:17579662-Receptors, Vasopressin,
pubmed-meshheading:17579662-Sleep
|
pubmed:year |
2007
|
pubmed:articleTitle |
The role of the BK channel in potassium homeostasis and flow-induced renal potassium excretion.
|
pubmed:affiliation |
Institute of Pharmacology and Toxicology, Medical Faculty of the Eberhard Karls University, Wilhelmstrasse 56, 72074 Tübingen, Germany.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|