Document Detail

Cell-volume regulation by swelling-activated chloride current in guinea-pig ventricular myocytes.
MedLine Citation:
PMID:  15040846     Owner:  NLM     Status:  MEDLINE    
The cell-volume regulation by swelling-activated Cl- current (I(Cl,swell)) was studied in guinea pig ventricular myocytes, using a microscopic video-image analysis. We have previously shown that in ventricular cells depolarized in high-K+ ([K+]o>45 mM) solution, an activation of the cyclic AMP-dependent Cl- current (I(Cl,cAMP)) leads to cell swelling. We first investigated the mechanism underlying the I(Cl,cAMP)-independent recovery (shrinkage) of the swollen cells. They shrank when the membrane potential (Vm) was made negative to the equilibrium potential of Cl- (ECl) by lowering [K+]o or [Cl-]o in the high-K+ solution. This shrinkage was attenuated by the inhibitors (DIDS, glibenclamide, furosemide) of swelling-activated Cl- current (I(Cl,swell)). These findings suggested an involvement of I(Cl,swell) in the observed isosmotic cell shrinkage. On the other hand, an application of hyposmotic (70% of control) solution to the cells at normal [K+]o (ECl>Vm) induced a cell swelling, and the swollen cells underwent a slight but definite spontaneous cell shrinkage during hyposmotic challenge, indicating the operation of the mechanism of regulatory volume decrease (RVD). This RVD was pronounced at low [Cl-]o, at which ECl was much more positive than Vm. On the contrary, when the hyposmotic solution was applied to the cells at high [K+]o, at which ECl was negative to Vm, the cells swelled vigorously and monotonically without showing RVD, the swelling being much greater than that seen at normal [K+]o. Both the RVD at normal [K+]o and the extra cell swelling at high [K+]o were suppressed by DIDS. These results suggest that I(Cl,swell) activated by cell swelling can shrink or inflate the cardiac cells under hyposmotic as well as isosmotic conditions, depending on Vm and ECl.
Shintaro Yamamoto; Keiko Ishihara; Tsuguhisa Ehara; Takao Shioya
Related Documents :
19873446 - Water relations in the cell : i. the chloroplasts of nitella and of spirogyra.
7539086 - Stretch-activated channel blockers modulate cell volume in cardiac ventricular myocytes.
10484326 - Separate taurine and chloride efflux pathways activated during regulatory volume decrease.
1375516 - Fluid transport in a cultured cell model of kidney epithelial cyst enlargement.
17305716 - Establishment of porcine pulp-derived cell lines and expression of recombinant dentin s...
3938086 - Receptors and recognition mechanisms of trypanosoma cruzi.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Japanese journal of physiology     Volume:  54     ISSN:  0021-521X     ISO Abbreviation:  Jpn. J. Physiol.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-03-25     Completed Date:  2004-12-08     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  2985184R     Medline TA:  Jpn J Physiol     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  31-8     Citation Subset:  IM    
Department of Physiology, Saga Medical School, Saga, 849-8501 Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cell Membrane Permeability / drug effects,  physiology
Cell Size / drug effects
Chloride Channels / physiology*
Chlorine / metabolism*
Epinephrine / pharmacology
Guinea Pigs
Heart Ventricles / cytology,  drug effects
Ion Channel Gating / physiology*
Myocytes, Cardiac / cytology*,  drug effects,  physiology*
Osmotic Pressure / drug effects
Ventricular Function
Water-Electrolyte Balance / drug effects,  physiology*
Reg. No./Substance:
0/Chloride Channels; 51-43-4/Epinephrine; 7782-50-5/Chlorine

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

Previous Document:  Identification of caspase-independent PKCepsilon-JNK/p38 MAPK signaling module in response to metabo...
Next Document:  Verapamil prevents impairment in filterability of human erythrocytes exposed to oxidative stress.