Antagonist | No Antagonist1-b | With Antagonist1-b | ||||
---|---|---|---|---|---|---|
Control | Nociceptin | % inhibition | Nociceptin | % inhibition | n | |
(% contraction) | (% contraction) | |||||
Naloxone (10 μM) | 17.8 ± 4.2 | 7.4 ± 2.6 | 58.0 ± 12.8*1-c | 7.1 ± 3.2 | 61.2 ± 16.0* | 4 |
Nor-binaltorphimine (100 nM) | 16.3 ± 3.8 | 5.1 ± 2.0 | 71.3 ± 7.8* | 3.6 ± 1.7 | 80.9 ± 5.5* | 4 |
Naltrindole (100 nM) | 13.0 ± 3.1 | 8.8 ± 2.5 | 34.1 ± 3.9* | 5.8 ± 2.0 | 58.1 ± 7.9* | 3 |
↵1-a Guinea pig isolated bronchi were pretreated with propranolol, atropine and indomethacin. Contractions were evoked by EFS (1-ms pulse duration, 5 Hz, 20 V, 15-s train) and expressed as a percentage of the contraction elicited by barium chloride added at the end of the experiment.
↵1-b The electrical stimulations were delivered at 20-min intervals. The average response of the first two stimulations was taken as the control response. After the second EFS response had returned to base line, a single concentration of nociceptin (0.1 μM) was added to the tissue bath, and 15 min later the tissue was again stimulated with EFS. After the third EFS stimulation (in the presence of nociceptin, the opioid receptor antagonist was added to the tissue for 20 min, and a final EFS was delivered. Note that none of the antagonist treatments was capable of reversing the inhibition caused by nociceptin.
↵1-c An asterisk denotes where nociceptin (0.1 μM) caused a significant (P < .05) inhibition of the contraction.