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Am J Physiol Renal Physiol (July 18, 2006). doi:10.1152/ajprenal.00177.2006
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Submitted on May 23, 2006
Accepted on July 12, 2006

Myogenic Vasoconstriction in Mouse Renal Interlobar Arteries: Role of Endogenous {beta} and {gamma}ENaC

Nikki L Jernigan1 and Heather A Drummond1*

1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, United States

* To whom correspondence should be addressed. E-mail: hdrummond{at}physiology.umsmed.edu.

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; 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 {gamma}ENaC, using dominant-negative (DN) or small interfering RNA (siRNA) molecules, inhibits pressure-induced vasoconstriction in mouse renal interlobar arteries. To address this goal, isolated arteries were transiently transfected with {beta}or {gamma}ENaC DN-cDNA or siRNA molecules. Following 24 hrs, 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 {beta}ENaC DN-cDNA or siRNA suppresses {beta}-, but not {gamma}ENaC protein expression. Similarly, {gamma}ENaC DN-cDNA or siRNA suppresses {gamma}-, but not {beta}ENaC protein expression. In addition, transfection of {beta}- or {gamma}ENaC 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 {gamma}ENaC proteins are essential in mediating myogenic vasoconstriction in mouse renal interlobar arteries.




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