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1 Department of Biomedical Sciences, Physiology, and Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
* To whom correspondence should be addressed. E-mail: woodmanc{at}missouri.edu.
We tested the hypothesis that increased intraluminal shear stress induces endothelial nitric oxide synthase (eNOS) mRNA expression and improves endothelium-dependent dilation in senescent soleus muscle feed arteries (SFA) by increasing nitric oxide (NO) production. SFA were isolated from young (4 mo) and old (24 mo) male Fischer 344 rats and cannulated with two resistance matched glass micropipettes. SFA were exposed to no flow (NF), low flow (LF), intermediate flow (IF), or high flow (HF) for 4-hr. Mean intraluminal shear stress ranged from 0-82 dyn/cm2. At the end of the 4-hr treatment period, eNOS mRNA expression was assessed in each SFA. eNOS mRNA expression was significantly lower in old NF SFA than in young NF SFA. In old SFA, eNOS mRNA expression was induced in by IF (+154%) and HF (+136%) resulting in a level of expression that was not different from young SFA. In a separate series of experiments, SFA were pre-treated with NF or HF for 4-hr and endothelial function was assessed by examining vasodilator responses to acetylcholine (ACh). ACh-induced dilation was less in old NF SFA than young NF SFA. Pre-treatment with HF improved ACh-induced dilation in old SFA such that the response was similar to young SFA. In the presence of N
-nitro-L-arginine (L-NNA) to inhibit NOS, ACh-induced dilation was inhibited in old HF SFA such that the response was no longer greater than old NF SFA. These results indicate that increased intraluminal shear stress induces eNOS mRNA expression and improves endothelium-dependent dilation in senescent SFA by increasing NO production.
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