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Departments of Veterinary Biomedical Sciences and Medical Physiology and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211
We tested the
hypothesis that hindlimb unweighting (HLU) and the associated reduction
in soleus muscle blood flow causes decreased expression of endothelial
cell nitric oxide synthase (ecNOS) mRNA and protein and attenuated
endothelium-dependent vasodilator responses in rat soleus feed arteries
(SFA). Male Sprague-Dawley rats were exposed to HLU
(n = 12) or cage control (Con;
n = 12) conditions for 14 days. At the
end of this period, SFA were isolated, removed, and cannulated with two
glass micropipettes for examination of vasodilator responses or frozen
for analysis of ecNOS mRNA and protein expression. RT-PCR of RNA from
single SFA was used to measure ecNOS mRNA, and immunoblots on single
SFAs were used to measure ecNOS protein content. Results revealed that
both ecNOS mRNA and ecNOS protein expression were lower in SFA from HLU
rats. Dilation to increased intraluminal flow was attenuated in SFA from HLU rats (Con: 88 ± 8% vs. HLU: 53 ± 8%) as was maximal
vasodilation to acetylcholine
(10
9-104
M; Con: 88 ± 5% vs. HLU: 73 ± 5%). Sensitivity to the
endothelium-independent vasodilator sodium nitroprusside
(1010-104
M) was enhanced by HLU (EC50: Con:
4.46 × 107 M vs. HLU:
5.00 × 108 M).
Collectively, these data indicate that the chronic reduction in soleus
blood flow associated with the reduced physical activity during HLU
results in reduced expression of ecNOS mRNA and protein in SFA and
attenuated endothelium-dependent vasodilation.
microcirculation; acetylcholine; flow-induced dilation; sodium nitroprusside; microgravity
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