Is There Attenuation of Non-Adrenergic Vasoconstriction in Active Skeletal Muscle?

Studies performed in our laboratory in conscious animals, demonstrate that the responsiveness of α-adrenergic receptors on the arterial vasculature of skeletal muscle is reduced during dynamic exercise compared to rest. A classical view of sympathetic vasoconstriction describes the release of norepinephrine (NE) which binds postsynaptic α-adrenergic receptors. There are two distinct populations of α-adrenergic receptors (α₁ and α₂) found of vascular smooth muscle, both of which produce vasoconstriction when stimulated. We have shown an attenuation of vasoconstriction during exercise with simultaneous stimulation of both populations of receptors. When examining the contribution of α₁ and α₂ receptors individually, α₂ receptors appear to be much more sensitive to attenuation by exercise than α₁ receptors. Existing evidence suggests that ATP acts as a neurotransmitter in vascular smooth muscle and is co-released with norepinephrine from sympathetic nerves. Recently we have examined P2X purinergic receptor responsiveness in the vasculature of exercising skeletal muscle. As with α-adrenergic receptors, P2X receptor responsiveness was attenuated during exercise compared to rest. These studies provide convincing evidence that the same sympathetic stimulation in resting skeletal muscle produces more vasoconstriction than in exercising skeletal muscle. Furthermore, there appears to be an inverse relationship between exercise intensity and the magnitude of constriction produced with sympathetic stimulation of the arterial vasculature of skeletal muscle. Supported by NIH and VA Medical Research Service