Nicotine and Tobacco

Drug Class: CNS Stimulant
Chemical Structure: The empirical formula is C10H14N2
Nicotine

Drug Combinations:
Street drug users sometimes mix tobacco with other drugs such as cannabis or phencyclidine (PCP) and smoke the combination. A majority of alcoholics and alcohol abusers smoke as well. It has been shown that smoking enhances the metabolism of some other drugs, including antidepressants. This effect is from tar in the cigarette and not the nicotine.

Pharmacokinetics:
Nicotine is readily absorbed from the respiratory tract, buccal membranes and skin. 80-90% of nicotine is metabolized in the body mainly by the liver, but also by the kidney and lung. The major metabolites of nicotine are cotinine and 1-N-nicotine oxide. In the body, the half-life of nicotine is about 2 hours while the half-life of its major metabolite is about 18 hours. Both nicotine and its metabolites are eliminated by the kidney. Nicotine is also excreted in the milk of lactating women who smoke.

Pharmacologic actions:
Nicotine activates cholinergic receptors directly, and it produces a wide cascade of physiologic actions. Among these is the release of neurotransmitter and hormones but especially catecholamines. The release of epinephrine by nicotine especially from adrenal medulla, causes an increase in free fatty acids, glycerol, and lactate concentrations in the blood. Nicotine stimulates the release of a varieity of pituitary hormones, including adrenocorticotropic hormone (ACTH), prolactin, growth hormone, and vasopressin. All nicotinic effects appear to be blocked by drugs such as mecamylamine, a non-competitive blocker that occupies the ion channel and not the nicotinic binding site.

Lethality:
There is a long latency to disease ( several decades for cancer and atherosclerotic disease). However, approximately 390,000 deaths/year in the US are attributed to smoking. A lethal dose in adults is estimated to be approximately 60 mg. A few drops of pure nicotine on the tongue would quickly kill a healthy adult.

Tolerance and dependence:
Tolerance is seen in both experimental animals and humans after a single dose of nicotine. Tolerance is regarded as a clinical manifestation of neuronal adaptation to nicotine. Nicotine receptors are upregulated in the brains of smokers.

Withdrawal syndromes:
Withdrawal syndromes occur upon stopping regular tobacco consumption. In humans, the syndrome may begin within a few hours after the last dose and may continue for several weeks. Tobacco withdrawal, although distressing, is not life-threatening. Signs include craving for nicotine, irritability, frustration, anxiety, depression and increase in appetite.

Reinforcing Effects:
Nicotine fosters its own administration by both positive and negative reinforcement. The potential for nicotine to induce pleasurable subjective states or "euphoria" is considered positive reinforcement. Relief of withdrawal is the most recognized negative reinforcement. Its reinforcing actions are thought to be related to the central stimulation of nicotinic cholinergic receptors which eventually leads to dopamine release. Both the dopaminergic and endorphinergic systems have been implicated in the reinforcing properties of nicotine.

Medical use:
Gum and patches containing nicotine are used as substitutes for smoking or chewing tobacco by addicts attempting to quit.