Skeletal muscle depends on its arteriole network to meet metabolic demands during physical activity. However, inflammatory mediators can disrupt intercellular communication along arterioles, impairing blood flow regulation and thus negatively impact muscle function. This project evaluated arteriole responsiveness in the gluteus maximus (a locomotory muscle) of C57/BL6 mice in vivo using intravital microscopic techniques. Arterioles were demonstrated as functional using specific endothelial and smooth muscle cell specific reagents. Inducing inflammation with platelet activating factor (PAF) gave rise to an increased degree of arteriolar vasoconstriction as its concentration increased. In contrast, vasodilation transitioned to vasoconstriction as histamine concentration increased. However, the arteriolar effects of histamine were attenuated during NO inhibition with N[superscript omega]-nitro-L-arginine methyl ester (L-NAME), illustrating a NO-related mechanism. Therefore, our study established the gluteus maximus as a viable candidate for inflammatory studies related to locomotion, so that the links between physical activity, inflammation, and microvascular health may be investigated. --P. ii.
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