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Am J Physiol Heart Circ Physiol (December 2, 2004). doi:10.1152/ajpheart.00489.2004
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Submitted on May 27, 2004
Accepted on November 18, 2004

Time Course of Flow-Induced Vasodilation in Skeletal Muscle: Contributions of Dilator and Constrictor Mechanisms

Robert D Shipley1, Se Jeong Kim1, and Judy M Muller-Delp1*

1 Department of Health and Kinesiology, Texas A&M University, College Station, Texas, USA

* To whom correspondence should be addressed. E-mail: jmd{at}hlkn.tamu.edu.

The purpose of this study was to determine the time course of flow-induced vasodilation in soleus and gastrocnemius muscle arterioles, and the mechanisms that underlie vasodilatory responses to an increase in intraluminal flow. Vasodilation was assessed during twenty minutes of continuous exposure to intraluminal flow. Both soleus and gastrocnemius muscle arterioles dilated in response to flow, although the magnitude of vasodilation was greater in arterioles from the gastrocnemius muscle. Neither blockade of nitric oxide synthase with NG-nitro-L-arginine methyl ester (L-NAME) nor blockade of cyclooxygenase with indomethacin inhibited the initial vasodilation (0-2 min) in arterioles from either muscle. In contrast, vasodilation to sustained exposure to flow (2-20 min) was eliminated by treatment with L-NAME in arterioles from both muscles. Both depolarization with 40 mM KCl and blockade of KCa channels inhibited the initial flow-induced dilation, and the inhibition was greater in gastrocnemius muscle arterioles compared to soleus muscle arterioles. In the presence of L-NAME, prolonged exposure to flow resulted in constriction in soleus and gastrocnemius muscle arterioles. This constriction was abolished by endothelin receptor blockade. These results indicate that the time course and magnitude of flow-induced vasodilation differs between arterioles from soleus and gastrocnemius muscles. The immediate response to increased flow is greater in gastrocnemius muscle arterioles and involves activation of K+ channels. In arterioles from both soleus and gastrocnemius muscles, vasodilation to sustained flow exposure occurs primarily through production of nitric oxide. In the absence of nitric oxide, sustained exposure to flow results in pronounced constriction that is mediated by endothelin.




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