Abstract
This study was designed to determine whether shear-dependent changes in venular nitric oxide (NO) production can influence nearby arteriolar tone and whether this mechanism contributes to functional arteriolar dilation in contracting muscle. In resting spinotrapezius muscle of anesthetized rats, occlusion of one branch of an arcade venular bifurcation with divergent flow caused flow and wall shear rate in the parallel branch to increase by an average of 99 and 72%, respectively. After 10-30 s, the paired arcade arteriole dilated by an average of 30%, with a correlation between the increase in venular shear rate and the magnitude of arteriolar dilation. During muscle contraction, arcade arterioles dilated by 73-97% and arcade venular shear rate increased by 48-83%. The NO synthase inhibitor NG-monomethyl-L-arginine greatly attenuated arteriolar dilation to increased venular shear rate in resting muscle but did not affect arteriolar dilation in contracting muscle. These findings suggest that a shear-dependent increase in venular NO release can dilate nearby arterioles, but this mechanism is not important for the sustained dilation of these arterioles during functional hyperemia.
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