Journal of Applied Physiology AJP: Cell Physiology
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J Appl Physiol 92: 901-911, 2002; doi:10.1152/japplphysiol.00642.2001
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Vol. 92, Issue 3, 901-911, March 2002

Mechanisms of flow and ACh-induced dilation in rat soleus arterioles are altered by hindlimb unweighting

William G. Schrage1,2, Christopher R. Woodman2,3, and M. Harold Laughlin1,2,3

Departments of 1 Physiology and 2 Veterinary Biomedical Sciences, and 3 Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211

The purpose of this study was to test the hypothesis that endothelium-dependent dilation (flow-induced dilation and ACh-induced dilation) in rat soleus muscle arterioles is impaired by hindlimb unweighting (HLU). Male Sprague-Dawley rats (~300 g) were exposed to HLU or weight-bearing control (Con) conditions for 14 days. Soleus first-order (1A) and second-order (2A) arterioles were isolated, cannulated, and exposed to step increases in luminal flow at constant pressure. Flow-induced dilation was not impaired by HLU in 1A or 2A arterioles. The cyclooxygenase inhibitor indomethacin (Indo; 50 µM) did not alter flow-induced dilation in 1As or 2As. Inhibition of nitric oxide synthase (NOS) with Nomega -nitro-L-arginine (L-NNA; 300 µM) reduced flow-induced dilation by 65-70% in Con and HLU 1As. In contrast, L-NNA abolished flow-induced dilation in 2As from Con rats but had no effect in HLU 2As. Combined treatment with L-NNA + Indo reduced tone in 1As and 2As from Con rats, but flow-induced dilation in the presence of L-NNA + Indo was not different from responses without inhibitors in either Con or HLU 1As or 2As. HLU also did not impair ACh-induced dilation (10-9-10-4 M) in soleus 2As. L-NNA reduced ACh-induced dilation by ~40% in Con 2As but abolished dilation in HLU 2As. Indo did not alter ACh-induced dilation in Con or HLU 2As, whereas combined treatment with L-NNA + Indo abolished ACh-induced dilation in 2As from both groups. We conclude that flow-induced dilation (1As and 2As) was preserved after 2 wk HLU, but HLU decreased the contribution of NOS in mediating flow-induced dilation and increased the contribution of a NOS- and cyclooxygenase-independent mechanism (possibly endothelium-derived hyperpolarizing factor). In soleus 2As, ACh-induced dilation was preserved after 2-wk HLU but the contribution of NOS in mediating ACh-induced dilation was increased.

skeletal muscle; microcirculation; physical inactivity; simulated microgravity; reduced blood flow


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