The most prominent phytochemical found in "N. tabacum" is nicotine. Nicotine binds stereospecifically to acetylcholine receptors at the autonomic ganglia, adrenal medulla, neuromuscular junctions and the brain. As a consequence of the stimulation of nicotinic receptors, possibly located on presynaptic sites, short-term exposure to nicotine results in the activation of several central nervous system neurohumoral pathways, leading to the release of acetylcholine, norepinephrine, dopamine, serotonin, vasopressin, growth hormone, and ACTH.

Most of the effects of nicotine on the central nervous system are due to the direct action on brain receptors, although activation of the brain through afferent nerves of chemoreceptors in the carotid bodies or the lung may also contribute. Nicotine excites nicotinic receptors in the spinal cord, autonomic ganglia, and adrenal medulla, the last of which causes the release of epinephrine. Nicotine evokes the release of catecholamines and facilitates the release of electrical stimulation-evoked neurotransmitters from sympathetic nerves in blood vessels. In experimental preparations, nicotine in low doses causes ganglionic stimulation but in high doses it causes ganglionic blockade after brief stimulation. This biphasic response pattern is observed in the intact organism as well, although the mechanism is far more complex.

At very low doses, similar to those seen during cigarette smoking, the cardiovascular effects appear to be mediated by the central nervous system, either through the activation of chemoreceptor afferent pathways or by direct effects on the brain stem. The net result is sympathetic neural discharge, with an increase in blood pressure and heart rate. At higher doses, nicotine may act directly on the peripheral nervous system, producing ganglionic stimulation and the release of adrenal catecholamines. At extremely high doses, nicotine produces hypotension and slowing of the heart rate, mediated by either peripheral ganglionic blockade, vagal afferent nerve stimulation, or direct depressor effects mediated by action on the brain.
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