Nicotine

Buccal🕒 Plan

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Oral🕒 Plan

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Smoked🕒 Plan

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🧬 Receptor activityDC

Mechanism of actionPH

Nicotine is a stimulant drug that acts as an agonist at nicotinic acetylcholine receptors. These are ionotropic receptors composed up of five homomeric or heteromeric subunits. In the brain, nicotine binds to nicotinic acetylcholine receptors on dopaminergic neurons in the cortico-limbic pathways. This causes the channel to open and allow conductance of multiple cations including sodium, calcium, and potassium. This leads to depolarization, which activates voltage-gated calcium channels and allows more calcium to enter the axon terminal. Calcium stimulates vesicle trafficking towards the plasma membrane and the release of dopamine into the synapse. Dopamine binding to its receptors is responsible the euphoric and addictive properties of nicotine. Nicotine also binds to nicotinic acetylcholine receptors on the chromaffin cells in the adrenal medulla. Binding opens the ion channel allowing influx of sodium, causing depolarization of the cell, which activates voltage-gated calcium channels. Calcium triggers the release of epinephrine from intracellular vesicles into the bloodstream, which causes vasoconstriction, increased blood pressure, increased heart rate, and increased blood sugar.
Nicotine is a ganglionic (nicotinic) cholinergic-receptor agonist. The pharmacologic actions of nicotine are complex and include a variety of effects mediated by stereospecific binding to receptors in autonomic ganglia, the adrenal medulla, the neuromuscular junction, and the brain.
The principal pharmacologic effect of small doses of nicotine is initial, transient stimulation of autonomic ganglia; large doses or prolonged neuronal receptor exposure to nicotine results in subsequent persistent depression of receptor activity. Although nicotine has similar dose-related effects at the myoneural (neuromuscular) junction, rapidly developing skeletal muscle paralysis obscures the stimulant phase. The muscle-relaxant properties of nicotine may be mediated through stimulation of Renshaw cells and pulmonary afferent nerves, which results in inhibition of skeletal muscle motor activity; such relaxant effects may contribute to the behavior-reinforcing effects of the drug. Small doses of nicotine directly stimulate sympathetic ganglia and facilitate neurotransmission; however, large doses produce initial ganglionic stimulation, which is quickly followed by inhibition of neurotransmission.

PharmacodynamicsPH

Nicotine, the primary alkaloid in tobacco products binds stereo-selectively to nicotinic-cholinergic receptors on autonomic ganglia, the adrenal medulla, neuromuscular junctions and in the brain. Nicotine exerts two effects, a stimulant effect exerted at the locus ceruleus and a reward effect in the limbic system. Itranvenous administration of nicotine causes release of acetylcholine, norepinephrine, dopamine, serotonine, vasopressin, beta-endorphin and ACTH. Nicotine is a highly addictive substance. Nicotine also induces peripheral vasoconstriction, tachycardia and elevated blood pressure. Nicotine inhalers and patches are used to treat smoking withdrawl syndrome. Nicotine is classified as a stimulant of autonomic ganglia.

Pharmacokinetics

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