Document Detail


Potassium excretion through ROMK potassium channel expressed in gill mitochondrion-rich cells of Mozambique tilapia.
MedLine Citation:
PMID:  22204952     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Despite recent progress in physiology of fish ion homeostasis, the mechanism of plasma K+ regulation has remained unclear. Using Mozambique tilapia, a euryhaline teleost, we demonstrated that gill mitochondrion-rich (MR) cells were responsible for K+ excretion, using a newly invented technique that insolubilized and visualized K+ excreted from the gills. For a better understanding of the molecular mechanism of K+ excretion in the gills, cDNA sequences of renal outer medullary K+ channel (ROMK), potassium large conductance Ca(2+)-activated channel, subfamily M (Maxi-K), K(+)-Cl(-) cotransporters (KCC1, KCC2, and KCC4) were identified in tilapia as the candidate molecules that are involved in K+ handling. Among the cloned candidate molecules, only ROMK showed marked upregulation of mRNA levels in response to high external K+ concentration. In addition, immunofluorescence microscopy revealed that ROMK was localized in the apical opening of gill MR cells, and that the immunosignals were most intense in the fish acclimated to the environment with high K+ concentration. To confirm K+ excretion via ROMK, K+ insolubilization-visualization technique was applied again in combination with K+ channel blockers. The K+ precipitation was prevented in the presence of Ba2+, indicating that ROMK has a pivotal role in K+ excretion. The present study is the first to demonstrate that the fish excrete K+ from the gill MR cells, and that ROMK expressed in the apical opening of the MR cells is a main molecular pathway responsible for K+ excretion.
Authors:
Fumiya Furukawa; Soichi Watanabe; Satoshi Kimura; Toyoji Kaneko
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-12-28
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  302     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-06     Completed Date:  2012-05-03     Revised Date:  2012-05-23    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R568-76     Citation Subset:  IM    
Affiliation:
Department of Aquatic Bioscience, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo, Tokyo, Japan. fumiya@marine.fs.a.u-tokyo.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Gills / metabolism*
Homeostasis / physiology
Humans
Mitochondria / metabolism*
Molecular Sequence Data
Potassium / metabolism*
Potassium Channels, Calcium-Activated / metabolism
Potassium Channels, Inwardly Rectifying / analysis,  metabolism*
Rats
Symporters / metabolism
Tilapia / physiology*
Zebrafish
Chemical
Reg. No./Substance:
0/Potassium Channels, Calcium-Activated; 0/Potassium Channels, Inwardly Rectifying; 0/Symporters; 0/potassium-chloride symporters; 7440-09-7/Potassium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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