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Nicotine’s primary molecular target peripherally is the nicotinic acetylcholine receptor on autonomic ganglia and sensory nerves. Its action leads to neurotransmitter/neuropeptide release causing various physiological responses including cardiovascular stimulation and local irritation. Peripheral neutralization strategies focus on modifying nicotine’s chemical state or blocking its action at these sites—often using organic acids—to reduce unwanted side effects while maintaining efficacy for therapeutic applications like smoking cessation aids.
Agonism at nAChRs; possible antagonism via chemical modification
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