Hindlimb unweighting decreases endothelium-dependent dilation and enos
expression in soleus not gastrocnemius.
Woodman, Christopher R., William G. Schrage, James W. E. Rush, Chester A. Ray,
Elmer M. Price, Eileen M. Hasser, and M. Harold Laughlin.
Departments of Veterinary Biomedical Sciences and Physiology and The Dalton
Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211
APStracts 8:0291A, 2001.
We tested the hypothesis that hindlimb unweighting (HLU) decreases endothelium-
dependent vasodilation and expression of endothelial nitric oxide synthase (eNOS) and
superoxide dismutase-1 (SOD-1) in arteries of skeletal muscle with reduced blood flow
during HLU. Sprague-Dawley rats (300-350 g) were exposed to HLU (n = 15) or control
(n = 15) conditions for 14 days. ACh-induced dilation was assessed in muscle with
reduced (soleus; Sol) or unchanged (gastrocnemius; Gast) blood flow during HLU. eNOS
and SOD-1 expression were measured in feed arteries (FA), first-order (1A), second-
order (2A), and third-order (3A) arterioles. Dilation to infusion of ACh in vivo was
blunted in Sol but not Gast. In arteries of Sol muscle, HLU decreased eNOS mRNA and
protein content. eNOS mRNA content was significantly less in Sol FA (35%), 1A
arterioles (25%) and 2A arterioles (18%). eNOS protein content was less in Sol FA
(64%) and 1A arterioles (65%) from HLU rats. In arteries of Gast, HLU did not decrease
eNOS message or protein. SOD-1 mRNA expression was less in Sol 2A arterioles (31%)
and 3A arterioles (29%) of HLU rats. SOD-1 protein content was less in Sol FA (67%)
but not arterioles. SOD-1 mRNA and protein content were not decreased in arteries from
Gast. These data indicate that HLU decreases endothelium-dependent vasodilation, eNOS
expression, and SOD-1 expression primarily in arteries of Sol muscle where blood flow is
reduced during HLU.
Received 25 January 2001; accepted in final form 1 May 2001
APS Manuscript Number A73-1.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 18 June 2001