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In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-microm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10(-4) M, 0.6 s) spread to, but not beyond, the area of damage. Taken together, these data provide strong evidence that conducted vasomotor responses have an important role in coordinating blood flow in response to an arteriolar occlusion.

Original publication




Journal article


Am J Physiol Heart Circ Physiol

Publication Date





H279 - H284


Acetylcholine, Animals, Arterioles, Blood Flow Velocity, Endothelium, Vascular, Indomethacin, Male, Microcirculation, Muscle, Skeletal, Muscle, Smooth, Vascular, NG-Nitroarginine Methyl Ester, Rats, Rats, Sprague-Dawley, Stress, Mechanical, Vasodilation