Document Detail

Swelling-activated cation channels mediate depolarization of rat cerebrovascular smooth muscle by hyposmolarity and intravascular pressure.
MedLine Citation:
PMID:  10944177     Owner:  NLM     Status:  MEDLINE    
1. Increases in intravascular pressure depolarize vascular smooth muscle cells. Based on the attenuating effects of Cl- channel antagonists, it has been suggested that swelling-activated Cl- channels may be integral to this response. Consequently, this study tested for the presence of a swelling-activated Cl- conductance in both intact rat cerebral arteries and isolated rat smooth muscle cells. 2. A 50 mosmol l-1 hyposmotic challenge (300 to 250 mosmol l-1) constricted rat cerebral arteries. This constriction contained all the salient features of a pressure-induced response including smooth muscle cell depolarization and a rise in intracellular Ca2+ that was blocked by voltage-operated Ca2+ channel antagonists. The hyposmotically induced depolarization was attenuated by DIDS (300 microM) and tamoxifen (1 microM), a response consistent with the presence of a swelling-activated Cl- conductance. 3. A swelling-activated current was identified in cerebral vascular smooth muscle cells. This current was sensitive to Cl- channel antagonists including DIDS (300 microM), tamoxifen (1 microM) and IAA-94 (100 microM). However, contrary to expectations, the reversal potential of this swelling-activated current shifted with the Na+ equilibrium potential and not the Cl- equilibrium potential, indicating that the swelling-activated current was carried by cations and not anions. The swelling-activated cation current was blocked by Gd3+, a cation channel antagonist. 4. Gd3+ also blocked both swelling- and pressure-induced depolarization of smooth muscle cells in intact cerebral arteries. 5. These findings suggest that swelling- and pressure-induced depolarization arise from the activation of a cation conductance. This current is inhibited by DIDS, tamoxifen, IAA-94 and gadolinium.
D G Welsh; M T Nelson; D M Eckman; J E Brayden
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  527 Pt 1     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2000 Aug 
Date Detail:
Created Date:  2000-10-05     Completed Date:  2000-11-07     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  139-48     Citation Subset:  IM    
Department of Pharmacology, University of Vermont, Burlington, VT 05405, USA.
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MeSH Terms
Brain / blood supply,  physiology
Calcium Channel Blockers / pharmacology
Calcium Channels / drug effects,  metabolism
Cations / metabolism*
Cells, Cultured
Cerebral Arteries / drug effects,  physiology*
Chloride Channels / antagonists & inhibitors,  metabolism*,  physiology*
Electric Conductivity*
Gadolinium / pharmacology
Ion Channels / drug effects,  metabolism*,  physiology*
Membrane Potentials
Muscle, Smooth, Vascular / drug effects,  physiology*
Osmolar Concentration*
Rats, Sprague-Dawley
Sodium / metabolism
Tamoxifen / pharmacology
Vasoconstriction / drug effects,  physiology*
Grant Support
Reg. No./Substance:
0/Calcium Channel Blockers; 0/Calcium Channels; 0/Cations; 0/Chloride Channels; 0/Ion Channels; 10540-29-1/Tamoxifen; 7440-23-5/Sodium; 7440-54-2/Gadolinium

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

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