ABSTRACT
BACKGROUNDS: Pain can occur following acute noxious stimuli and tissue damage. The duration of such pain may outlast the stimulus and its amplitude may be exaggerated (hyperalgesia). This response comes from a sensitization of the peripheral nociceptor. Traditional thought has associated the antinociceptive effects of opiates with the activation of opioid receptors located in the central nervous system. Recently, however, opiate receptors in the peripheral nervous system have led to the hypothesis that analgesic action might, in part, result from a reduction in the response of peripheral nerve fibers thought to be concerned with signaling pain. METHODS: Twenty units were recorded from the strands of the hypogastric nerve innervating the urinary bladder of the cat. Nerve activity and intravesical pressure were monitored before and after the onset of an acute inflammation induced by the intravesical instillation of 2% mustard oil. The responses of afferent units to chemical stimuli by intra-arterially injected bradykinin (10 microgram/0.2 ml., i.a.) and potassium chloride (0.3 M/0.2 ml, i.a.) were compared each time at control, after inflammation, and after administration of morphine (2.5 mg/kg) and naloxone (5 microgram/kg) respectively. RESULTS: Polymodal receptors in the urinary bladder showed excitatory response to algesic substances such as bradykinin, potassium chloride and the urinary bladder contracted simultaneously, both the responses of the nerve impulse and bladder contraction to bradykinin and potassium chloride increased significantly after bladder inflammation induced by 2% mustard oil and the sensitization of the sensory receptors attenuated by morphine and naloxone reversed the effect of morphine. CONCLUSIONS: These observations suggest that morphine might have a peripheral effect.