Flow‐Dependent Dilation and Myogenic Constriction Interact to Establish the Resistance of Skeletal Muscle Arterioles

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Abstract
Objective: To test the hypothesis that the diameter of skeletal muscle arterioles is determined by the interaction of responses elicited by intravascular pressure and flow.Methods: Experiments were conducted on isolated, cannulated, first‐order arterioles of cremaster muscle of male Wistar rats. The diameter of arterioles was followed by videomicroscopy. Perfusion pressures and flows were controlled.Results: In the absence of perfusate flow, increases in perfusion pressure (from 0 to 120 mm Hg), after initial dilation, elicited endothelium independent constrictions of arterioles. At 60 mm Hg of perfusion pressure, the active diameter of vessels was 84.9 ± 1.9 μm. The passive diameter of arterioles (Ca2+‐free solution) was 150.6 ± 2.4 μm. Increases in perfusate flow resulted in a significant upward shift in the pressure—diameter curves; in the presence of perfusate flows of 20, 40, and 60 μL/min, the constriction of the vessels at a pressure of 60 mm Hg was attenuated by 25.1 ± 3.9%, 35.2 ± 3.0%, and 46.8 ± 4.4%, respectively. In contrast, the corresponding diameter of arterioles at perfusate flows of 10 to 60 μL/min was significantly reduced when perfusion pressure was increased from 60 to 80 and 100 mm Hg (at a flow of 60 μL/min) by 12.0 ± 4.3% and 37.1 ± 2.8%, respectively. Hence, both flow‐ and shear stress—diameter curves were significantly shifted downward when perfusion pressure increased from 60 to 100 mm Hg.Conclusion: These results demonstrate that an interplay between pressure and flow‐sensitive mechanisms is an important determinant of the arteriolar resistance in skeletal muscle.