Role of Endothelial Nitric Oxide in Control of Peripheral Vascular Conductance During Muscle Metaboreflex Activation

Muscle metaboreflex activation during submaximal dynamic exercise, increases arterial pressure primarily via increases in cardiac output as there is little systemic vasoconstriction. Indeed, in normal animals we have often shown a small, but significant, peripheral vasodilation during metaboreflex activation, which is mediated, at least in part, by release of epinephrine and activation of vascular β₂ receptors. We tested whether this vasodilation is in part due to increased release of nitric oxide caused by the rise in cardiac output eliciting endothelium-dependent flow-mediated vasodilation. The muscle metaboreflex was activated via graded reductions in hindlimb blood flow during mild exercise with and without nitric oxide synthesis blockade (L-nitroarginine methyl ester (L-name); 5mg/kg). We assessed the role of increased cardiac output in mediating peripheral vasodilation via the slope of the relationship between the rise in non-ischemic vascular conductance (conductance of all vascular beds excluding hindlimbs) vs. the rise in cardiac output. L-name increased mean arterial pressure at rest and during exercise. The metaboreflex-induced increases in mean arterial pressure were unaltered by L-name; whereas, the increases in cardiac output and non-ischemic vascular conductance were attenuated. However, the slope of the relationship between non-ischemic vascular conductance and cardiac output was not affected by L-name indicating that the rise in cardiac output did not elicit vasodilation via increased release of nitric oxide. Thus, although nitric oxide is intrinsic to the vascular tonus, endothelial-dependent flow-mediated vasodilation plays little role in the small peripheral vasodilation observed during muscle metaboreflex activation.

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