What is the pharmacology of cocaine toxicity?

Updated: Sep 01, 2018
  • Author: Lynn Barkley Burnett, MD, EdD, LLB(c); Chief Editor: Sage W Wiener, MD  more...
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Answer

The chemical name for cocaine is benzoylmethylecgonine. It is derived from the leaves of Erythroxylon coca, a shrub indigenous to Peru, Bolivia, Mexico, the West Indies, and Indonesia. Cocaine is a bitter crystalline alkaloid with the molecular formula of C17 H21 NO4. Ecgonine, an important part of the cocaine molecule, is an ester-type local anesthetic that belongs to the tropane family, which also includes atropine and scopolamine.

The primary effect of cocaine is blockade of norepinephrine reuptake; its secondary effect is marked release of norepinephrine. These effects act synergistically to increase norepinephrine levels at the nerve terminal. Cocaine also causes moderate release and reuptake-blockade of serotonin and dopamine. Its marked local anesthetic effects are caused by sodium channel blockade, which inhibits the conduction of nerve impulses, decreasing the resting membrane potential and the amplitude of the action potential while simultaneously prolonging the duration of the action potential. In the heart, cocaine acts as a Vaughan Willaims IC sodium channel blocker.

Cocaine also blocks potassium channels. In some cellular membranes, it may block sodium-calcium exchange. The drug is fat soluble and freely crosses the blood-brain barrier. Cocaine appears to stimulate the CNS, with particular activity in the limbic system. There, it potentiates dopaminergic transmission in the ventral basal nuclei, producing the pleasurable behavioral effects that result in its widespread use.


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