Abstract

The effects of HC-3, reserpine, guanethidine, hexamethonium, gallamine and atropine were tested on the response of the perfused dog hind leg and perfused "gracilis muscle" in situ to nerve stimulation, nicotine, acetylcholine and norepinephrine. HC-3 was ineffective in inhibiting the vasoconstriction following sympathetic nerve stimulation, but it was effective in blocking the vasodilatation which occurred following stimulation of the same nerve in acutely "reserpinized" preparations. These findings suggest the existence of separate cholinergic and adrenergic components in the sympathetic innervation to the vascular bed of the hind limb of the dog rather than a cholinergic junction in the adrenergic fibers.

The evidence is compatible with a local, cholinergic-adrenergic interaction between the distinct cholinergic and adrenergic fibers in the sympathetic innervation to these vascular beds. HC-3 was ineffective in inhibiting the vasodilatation due to stimulation of somatic fibers in the perfused "gracilis muscle" preparation in situ at a time when inhibition of the vasodilatation following sympathetic nerve stimulation was complete. Nicotine produced a vasodilatation in these preparations. This response was not inhibited by HC-3 although HC-3 has been reported to be effective in blocking the response to nicotine in other preparations.

These last two findings have been discussed in relation to the hypothesis that the postganglionic mechanism of nicotine could be mediated via a eholinergic mechanism through release of endogenous stores of acetyicholine. A possible role of the neuroeffector junction of the somatic nervous system as a site of these endogenous stores of acetylcholine is postulated.