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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

A novel approach to the pharmacology of analgesics.

To date in the United States when a patient has presented with a complaint of pain requiring some form of pharmacologic relief, the physician has had the choice of two broad classes of drugs: peripherally acting (i.e., NSAID) or centrally acting (i.e., opioid) analgesics. The antidepressant monoamine reuptake inhibitors, particularly when combined with an opioid analgesic, have also proven efficacious in treating certain types of pain conditions. A new approach, available for almost 20 years in Europe and recently approved for use in the United States, is the centrally acting synthetic analgesic tramadol HCI. Preclinical evidence suggests that tramadol produces its antinociceptive effect in animals and analgesic effect in humans through a complementary dual mechanism of action. One mechanism relates to its weak affinity for mu-opioid receptors (6,000-fold less than morphine, 100-fold less than d-propoxyphene, 10-fold less than codeine, and equivalent to dextromethorphan). A metabolite (O-desmethyltramadol; M1) binds to opioid receptors with a greater affinity than the parent compound and could contribute to this component. However, in most animal tests and human clinical trials, the analgesic effect of tramadol is only partially blocked by the opioid antagonist naloxone, suggesting an important nonopioid mechanism. This nonopioid mechanism possibly relates to an increase in central neuronal synaptic levels of two neurotransmitters, 5-hydroxytryptamine (5-HT; serotonin) and norepinephrine. The opioid and nonopioid mechanisms appear to combine in a supra-additive manner in several tests of antinociception, but only in an additive or even counteracting manner in measures of adverse-effect liability. In sum, the apparent dual mechanism of action of tramadol suggests a possible new approach to pain relief.[1]

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