Autonomic nervous system

Parasympathetic division. Stimulation of cholino-ceptors in autonomic ganglia and at the post ganglionic endings affects chiefly the following organs:

Eye: miosis and spasm of the ciliary muscle occur so that the eye is accommodated for near vision. Intraocular pressure falls due, perhaps, to dilation of vessels at the point where intraocular fluids pass into the blood.

Exocrine glands: there is increased secretion most noticeably of the salivary, lachrymal, bronchial and sweat glands. The last are cholinergic, although anatomically part of the sympathetic system; some sweat glands, e.g. axillary, may be adrenergic.

Heart: bradycardia occurs with atrioventricular block and eventually cardiac arrest.

Bronchi: there is bronchoconstriction and mucosal hypersecretion that may be clinically serious in asthmatic subjects, in whom cholinergic drugs should be avoided, as far as possible.

Gut: motor activity is increased and may cause colicky pain. Exocrine secretion is also increased. Tone in sphincters falls which may cause defaecation (anal sphincter) or acid reflux/regurgitation (oesophageal sphincter).

Bladder and ureters contract and the drugs promote micturition.

Sympathetic division. The ganglia only are stimulated, also the cholinergic nerves to the adrenal medulla. These effects are overshadowed by effects on the parasympathetic system and are commonly evident only if atropine has been given to block the latter, when tachycardia, vasoconstriction and hypertension occur.

Neuromuscular (voluntary) junction

The neuromuscular junction has a cholinergic nerve ending and so is activated by anticholinesterases which allow acetylcholine to persist, causing muscle fasciculation. Prolonged activation leads to a secondary depolarising neuromuscular block.

Central nervous system

There is usually stimulation followed by depression but variation between drugs is great, possibly due to differences in CNS penetration. In overdose, mental excitement occurs, with confusion and restlessness, insomnia (with nightmares when sleep does come), tremors and dysarthria and sometimes even convulsions and coma.

Blood vessels

There is stimulation of cholinergic vasodilator nerve endings in addition to the more important dilating action on arterioles and capillaries mediated through noninnervated receptors. Anticholinesterases potentiate acetylcholine that exists in the vessel walls independently of nerves.

Nicotinic and muscarinic effects

It was Henry Dale, in 1914, who first made this functional division which remains a robust and useful way of classifying cholinergic drug effects. He noted that the actions of acetylcholine and substances acting like it at autonomic ganglia and the neuromuscular junction (i.e. at the end of cholinergic nerves arising within the central nervous system) mimic the stimulant effects of nicotine (hence nicotinic). In contrast, the actions at postganglionic cholinergic endings (parasympathetic endings plus the cholinergic sympathetic nerves to the sweat glands) and noninnervated receptors on blood vessels resembled the alkaloid, muscarine (hence muscarinic).

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