Document Detail

Myogenic vasoconstriction in mouse renal interlobar arteries: role of endogenous beta and gammaENaC.
MedLine Citation:
PMID:  16849693     Owner:  NLM     Status:  MEDLINE    
Mechanosensitive ion channels are thought to initiate pressure-induced vasoconstriction, however, the molecular identity of these channels is unknown. Recent work from our laboratory suggests that members of the Degenerin/Epithelial Na+ Channel (DEG/ENaC) family may be components of the mechanosensitive ion channel complex in vascular smooth muscle (VSM); however, the specific DEG/ENaC proteins mediating myogenic constriction are unknown. The goal of this study is to determine if specific knockdown of beta or gammaENaC, using dominant-negative (DN) or small-interference RNA (siRNA) molecules, inhibits pressure-induced vasoconstriction in mouse renal interlobar arteries. To address this goal, isolated arteries were transiently transfected with beta or gammaENaC DN-cDNA or siRNA molecules. After 24 h, vessels were either 1) cannulated and pressurized for pressure-diameter response curves or 2) dissociated and immunolabeled to determine VSM cell endogenous ENaC protein expression. We found that transfection of betaENaC DN-cDNA or siRNA suppresses beta-, but not gammaENaC protein expression. Similarly, gammaENaC DN-cDNA or siRNA suppresses gamma-, but not betaENaC protein expression. In addition, transfection of beta- or gammaENaC DN-cDNA or siRNA molecules inhibits pressure-induced vasoconstriction, but does not block agonist-induced vasoconstriction. Our results provide the first direct evidence that beta and gammaENaC proteins are essential in mediating myogenic vasoconstriction in mouse renal interlobar arteries.
Nikki L Jernigan; Heather A Drummond
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-07-18
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  291     ISSN:  1931-857X     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-11-03     Completed Date:  2007-01-05     Revised Date:  2011-04-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F1184-91     Citation Subset:  IM    
Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216, USA.
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MeSH Terms
Epithelial Sodium Channel / genetics*,  metabolism
Gene Expression
Kidney / blood supply*,  physiology
Mice, Inbred C57BL
Muscle, Smooth, Vascular / physiology*
RNA, Small Interfering
Renal Artery / physiology*
Vasoconstriction / physiology*
Grant Support
Reg. No./Substance:
0/Epithelial Sodium Channel; 0/RNA, Small Interfering; 0/Scnn1b protein, mouse; 0/Scnn1g protein, mouse

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