Key result
Methacholine increases carotid chemoreceptor discharge via nicotinic receptors in preclinical models.
Why the study?
The effects of methacholine on carotid chemoreceptors and the underlying receptor mechanisms were not fully understood.
Methacholine stimulates carotid chemoreceptors via nicotinic rather than muscarinic actions, supporting the principle that chemosensory activity is increased by nicotinic agonists.
Should not change clinical practice; extends nicotinic chemoreceptor activation principle in animal models and leaves open human translation.
The present electrophysiological study shows that methacholine (MCh), generally regarded as a muscarinic agonist, stimulates the carotid chemoreceptors in pentobarbitone anaesthetized cats. The response consisted of a primary increase in discharge, attributable to nicotinic actions of MCh since it was unaffected by atropine but abolished by mecamylamine, and a delayed secondary increase in discharge, due mainly to bronchoconstriction evoked by MCh. Physostigmine caused similar potentiation of responses to acetylcholine and MCh which implies that acetylcholinesterase is located close to the site(s) at which the drugs act to stimulate chemoreceptor activity. The findings are in agreement with the general principle that chemosensory activity is increased by nicotinic agonists but not by muscarinic agonists.
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Daniel S. McQueen (1978) studied this question. Methacholine was evaluated on Carotid chemoreceptor discharge. Methacholine stimulated carotid chemoreceptors in anaesthetized cats via nicotinic actions, causing an increase in discharge that was unaffected by atropine but abolished by mecamylamine.
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