Prostaglandins, pain, and inflammation.
The prevention of hyperalgesia by inhibition of prostaglandin synthesis is the most plausible hypothesis on the mechanism of NSAID action. This review also discusses other possibilities of controlling inflammatory hyperalgesia, including the development of peripherally acting opiates. These are obtained by reduction of the opiates' lipophilic properties. The drugs' undesired central effects are thus eliminated, while their peripheral analgesic action is preserved. Moreover, it appears that the adrenergic system is also involved in inflammatory hyperalgesia. This implies that beta-receptor blockers might be useful in eliminating the adrenergic component of inflammatory pain. Metamizol, in contrast to the NSAIDs, is effective even in manifest prostaglandin or sympathetic hyperalgesia.
D000262:Adenylyl Cyclases / Q000502:physiology; D004177:Dipyrone / Q000494:pharmacology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D010146:Pain / Q000503:physiopathology*; D011453:Prostaglandins / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology
D011453:Prostaglandins; D011943:Receptors, Adrenergic, beta; D004177:Dipyrone; D000262:Adenylyl Cyclases