NSAIDs -analgesic action
The way that NSAIDs produce analgesia may be different from the way they produce their anti-inflammatory effects. Both may be due to cyclo-oxygenase (COX) inhibition in various sites (althogh most NSAIDs have other effects which may also contribute to analgesia).
Steroids also reduce prostaglandin production (by acting higher up the cascade) but are not directly analgesic - they are potent anti-inflammatories and by removing inflammation they can reduce pain. NSAIDs are different in that they can produce analgesia in the absence of inflammation.
Prostaglandin receptor pharmacology is a developing field. The situation is confused at present; the receptors responsible for some effects (but not the sensitisation of neurones) have been elucidated. However, it is clear that PGD2, E2 and I2 can all sensitise peripheral neurones to the pain producing effects of bradykinin and other mediators.
Some (most??) analgesia may be produced in the CNS (probably the brain rather than the spinal cord). There is evidence that prostaglandins interact with several types of glutamate receptors to increase nociception, NSAIDs may block this.
All currently used drugs also have other effects unrelated to cyclo-oxygenase inhibition which could contribute to analgesia. Many scavenge free radicals, which will also reduce inflammation.
| 5 CNS index |
 |
 |
 |
 |
 |
 |
 |
copyright
Massey University
|