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Am J Physiol Renal Physiol (May 24, 2005). doi:10.1152/ajprenal.00019.2005
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Submitted on January 19, 2005
Accepted on May 20, 2005

Vascular ENaC Proteins are Required for Renal Myogenic Constriction

Nikki L. Jernigan1 and Heather A. Drummond1*

1 Department of Physiology and Biophysics and the Center for Excellence in Caediovascular Renal Research, University of Mississippi Medical Center, Jackson, MS, USA

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

The myogenic response is an essential component of renal blood flow autoregulation and is the inherent ability of vascular smooth muscle cells (VSMCs) to contract in response to increases in intraluminal pressure. Although mechanosensitive ion channels are thought to initiate VSMC stretch-induced contraction, their molecular identity is unknown. Recent reports suggest Degenerin/Epithelial Na+ Channels (DEG/ENaC) may form mechanotransducers in sensory neurons and VSMCs, however, the role of DEG/ENaC proteins in myogenic constriction of mouse renal arteries has not been established. To test the hypothesis DEG/ENaC proteins are required for myogenic constriction in renal vessels, we first determined expression of ENaC transcripts and proteins in mouse renal VSMCs (mrVSMCs). Then, we determined pressure- and agonist-induced constriction and changes in VSM cytosolic Ca2+ and Na+ in isolated mouse renal interlobar arteries following DEG/ENaC inhibition with amiloride and benzamil. We detect {alpha}-, {beta}-, and {gamma}ENaC transcript and protein expression in cultured mrVSMC. In contrast, we detect only {beta}- and {gamma}-, but not {alpha}-, ENaC protein in freshly dispersed mrVMSC. Selective DEG/ENaC inhibition, with low doses of amiloride and benzamil, abolish pressure-induced constriction and increases in cytosolic Ca2+ and Na+ without diminishing agonist-induced responses in isolated mouse interlobar arteries. Our findings indicate DEG/ENaC proteins are required for myogenic constriction in mouse interlobar arteries and are consistent with our hypothesis that DEG/ENaC proteins may be components of mechanosensitive ion channel complexes required for myogenic vasoconstriction.




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