Abstract

In contracting skeletal muscle, several vasoactive compounds have been proposed to override sympathetic vasoconstriction, a phenomenon termed functional sympatholysis. Adenosine triphosphate (ATP) has emerged as a candidate molecule capable of mediating these effects, however, the precise source and mechanisms have not been fully elucidated. We tested the hypothesis that endothelium mediated mechanisms are responsible for attenuating α‐adrenergic vasoconstriction. Experiments were conducted on 1A arterioles surgically dissected from the rat cremaster muscle. Sequential sections of arteriole were cannulated on glass micropipettes, pressurized to 70 mmHg, and warmed to 34°C in physiological saline solution. We measured changes in isolated vessel diameter in response to logarithmic concentrations of the α1‐adrenergic receptor specific agonist phenylephrine following dilatory responses to intraluminal flow (flow mediated dilation, n=12), intraluminal adenosine (n=10), or intraluminal ATP (n=11). All vessels tested spontaneously developed myogenic tone (>40% from initial diameter) and displayed functioning endothelium (>40% dilation to acetylcholine). Vessels dilated equally 177±19 μm, 183±10 μm, and 181±22 μm during flow mediated dilation, adenosine, and ATP, respectively. There were no significant differences between treatments following concentration‐response curves generated by phenylephrine administration and the EC50 was not different −5.90±0.02, −6.12±0.18, and −6.00±0.06 for flow mediated dilation, adenosine, or ATP (p=NS). Thus, there was no attenuation of α1‐adrenergic vasoconstriction in response to intraluminal flow mediated dilation, adenosine, or ATP in 1A arterioles. These results suggest that endothelium mediated dilation does not blunt α1‐adrenergic vasoconstriction in first order skeletal muscle arterioles.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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