Effects of Shear Stress on ecNOS Expression and Dilation in Soleus Feed Arteries
- Jeffrey Jasperse, Anatomy and Physiology Professor , Pepperdine University
- Jay Brewster, Cell Biology Professor, Pepperdine University
Shear stress causes artery dilation and increased expression of endothelial cell nitric oxide synthase (ecNOS) in coronary and placental arteries. We sought to determine the importance of shear stress in maintaining normal dilation and normal levels of ecNOS in rat soleus feed arteries (SFA). SFA were isolated from male Sprague-Dawley rats and cannulated for in vitro microscopy. SFA were exposed to no shear stress, low shear stress, or high shear stress conditions for 4 hours. After 4 hours, endothelium-dependent dilation (acetylcholine: ACh) and endothelium-independent dilation (sodium nitroprusside: SNP) were tested. Arteries were then uncannulated, mRNA was isolated, and RT-PCR for ecNOS mRNA was performed to determine whether shear stress altered ecNOS gene expression. Shear stress did not alter dilation to ACh, but dilation to SNP was greater in the high shear stress arteries. ecNOS mRNA content was greater in high shear stress arteries than low shear stress arteries. These data indicate that altered wall shear stress conditions alter ecNOS gene expression and vascular smooth muscle cell function.