Abstract
The hypothesis that sympathetic innervation to skeletal muscle vasculature contains functionally distinct adrenergic and cholinergic fibers was investigated utilizing the dog isolated perfused gracilis muscle. The use of hemicholinium in an attempt to abolish cholinergic dilatation, but not adrenergic constriction, in response to intermittent nerve stimulation was not successful. Continuous nerve stimulation produced vasoconstriction which was maintained for the duration of stimulation. Conversely, when cholinergic vasodilatation was unmasked, continuous stimulation resulted in a dilator response which disappeared rapidly. These experiments suggested that release of the adrenergic transmitter could not be dependent upon an intermediate cholinergic link in the sympathetic nerve. This postulate was supported further by experiments utilizing electrical stimulation of medullary vasoconstrictor areas. Whereas cholinergic vasodilatation was unmasked routinely by peripheral stimulation following reserpine, guanethidine or ß-TM 10, this response was never seen when medullary vasoconstrictor neurons were activated following these agents. It was concluded that sympathetic cholinergic nerves to skeletal muscle vessels possess a purely vasodilator function, and do not play an intermediate role involving release of the adrenergic transmitter.
Published Version
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