detoxified by plasma and hepatic cholinesterases to water soluble metabolites (2:299).
A powerful local anesthetic, cocaine exerts its effects through its ability to block the initiation and conduction of electrical impulses within the nerve cells (2:299). The drug blocks the presynaptic reuptake of the neurotransmitters norepinephrine and dopamine (6:487). Normally, presynaptic uptake is the mechanism by which postsynaptic stimulation is terminated (1:2470). Blockade of presynaptic reuptake results in the accumulation of the neurotransmitters at the postsynaptic receptor sites (2:299). This causes intense activation of postsynaptic nerve processes, and ultimately intense stimulation of the sympathetic nervous system (2:299).
In addition, neurotransmitter reuptake enables the chemicals to be stored and recycled in presynaptic nerve endings for future use (2:299). By blocking this recycling mechanism, cocaine use also results in gradual depletion the body's neurotransmitters (2:299). The intense craving for cocaine upon withdrawl is said to be related to this neurotransmitter depletion (2:299).
Over stimulation of the sympathetic nervous system has widespread physiologic consequences. Some of the systemic effects of cocaine include an acute rise in arterial blood pressure, tachycardia, predisposition to ventricular tachyarrhythmias, and seizures (2:299). Moreover, mydriasis, hyperglycemia, and hyperthermia may occur as well (2:299). Furthermore, vasoconstriction acts to prolong cocaine's absorption (2:299). Therefore cocaine slows its own metabolism (2:299). This actually magnifies the drug's adverse effects (2:299).
In addition to its systemic effects, cocaine can also cause widespread changes in the central nervous system. Initially, it causes an elevation in brain dopamine content (2:299 300). This phenomena may be largely responsible for the transient euphoria associated with the drug's use (2:299 300)....