Peripheral effects of nicotine and acetylcholine resembling those of sympathetic stimulation

Abstract

In this paper we extend observations which have been made on various peripheral effects of nicotine and acetylcholine, these being effects which resemble those of sympathetic stimulation. The pilomotor action of acetylcholine on the hairs of the cat's tail was described by von Briicke (1935); Coon & Rothman (1940) confirmed this and observed that nicotine had the same action. These workers began by studying the effect of acetylcholine in causing goose-flesh in the human forearm and then observed that small amounts of acetylcholine and of nicotine caused erection of tufts of hairs on the cat's tail after intradermal injection. They observed that the action was unaffected by atropine but was abolished by ergotamine. Kottegoda (1953a) described the action of nicotine and of acetylcholine in causing acceleration and increased contraction of isolated rabbit atria; he found these effects were best seen in the presence of atropine. In a second paper (Kottegoda, 1953b) he described the action of nicotine and of acetylcholine in causing vasoconstriction in the perfused vessels of the rabbit ear; he found that this vasoconstriction was reversed to vasodilatation when an agent which reversed the constrictor action of adrenaline was added to the perfusion fluid. Thus the effects of nicotine on the rabbit atria and the perfused rabbit ear resembled the effects of sympathetic stimulation and seemed to be due to the release of an adrenalinelike substance. More recently, Thompson (1955) found that nicotine caused a contraction of the isolated nictitating membrane of the cat. Further observations have now been made on the pilomotor response, on the response of the vessels of the perfused rabbit ear and on the response of the nictitating membrane.

Effect of Drugs on the Noradrenaline Content of Brain and Peripheral Tissues and Its Significance

“…This nicotine-like substance causes a stimulation of autonomic ganglia which is short-lived and not followed by paralysis (Chen & Portman, 1954); consequently, the same effect can be produced repeatedly, and the compound appeared ideally suited to test the hypothesis (Burn et al, 1959) that the action of nicotine on the vessels of the rabbit ear, the cat nictitating membrane and piloerectors, and other organs supplied with sympathetic fibres was produced indirectly by a release of noradrenaline and not due to a direct action of the drug on the ganglia. The site of the stores from which the noradrenaline would be released could be either the sympathetic neurones or the tissue itself.…”

Effects of nicotine on salivary amylase secretion from rabbit parotid gland

“…It can be considered that nicotine acts directly upon a-adrenoceptors as suggested by Burn, Leach, Rand & Thompson (1959) and Ferry (1963). The action of phenoxybenzamine on the flow rate can probably be explained as an inhibition of the direct action of nicotine, but the action of hexamethonium cannot be explained, and should be further investigated.…”

The effects of “autonomic drugs” on villous movement in the small intestine of the pigeon

“…It has been suggested that nicotine, in addition to its ganglion stimulating effect, can also have a direct action on smooth muscle, partly through an effect on the acetylcholine receptors and, to a lesser extent, on receptors sensitive to phenoxybenzamine (Day & Vane, 1963). In addition, it may liberate noradrenaline from peripheral stores (Burn, Leach, Rand & Thompson, 1959). Noradrenaline release by nicotine or an action of nicotine on phenoxybenzamine-Eensitive receptors did not seem to play a significant part in the present experiments as neither phenoxybenzamine nor tolazoline affected the response of the villi to nicotine.…”