AIM To study the antagonism of cholecystokinin octapeptide (CCK 8) against effect of morphine and its mechanism. METHODS The electrical and mechanical activities of rat duodenum in vitro were recorded simultan...AIM To study the antagonism of cholecystokinin octapeptide (CCK 8) against effect of morphine and its mechanism. METHODS The electrical and mechanical activities of rat duodenum in vitro were recorded simultaneously. RESULTS Acetylcholine (ACh) could increase the amplitude and the number of the spike potential (SPA and SPN) of rat duodenum in vitro , followed by the increase of the duodenal contraction amplitudes (CA), showing a positive correlation. Morphine, on the contrary, inhibited the potentiation of ACh, showing a negative correlation. CCK 8 could antagonize the effects of morphine, i.e. SPA and SPN were increased again, followed by the increase of CA. CCK A receptor antagonist Devazepide could reverse the antagonism of CCK 8 to the effect of morphine. CONCLUSION CCK 8 could antagonize the effect of morphine which inhibited the potentiation of ACh on the duodenal activities in vitro . The antagonistic effect of CCK 8 on morphine was mainly mediated by CCK A receptor.展开更多
Previous studies have shown that CCK-8 has distinct antiopioid effect in the central sites related with pain control and blood pressure control. The aim of this study was to explore the receptor mechanism by which CCK...Previous studies have shown that CCK-8 has distinct antiopioid effect in the central sites related with pain control and blood pressure control. The aim of this study was to explore the receptor mechanism by which CCK-8 antagonized the depressor effect of u-and k-opioid agonists, and to observe whether CCK-8 could antagonize the depressor effect induced by muscimol, a nonopioid substance. The results showed that (ⅰ) The antagonistic effect of CCK-8 on opioid-induced hypotension could be blocked by intrathecal (i.t.) administration of CCK-B antagonist L-365, 260 at nanogram doses, or by CCK-A antagonist devazepide at doses 20—40 times higher than L-365, 260, indicating that it was the CCK-B receptor which mediates the antiopioid effect. (ⅱ) The depressor effect induced by intrathecal muscimol, a GABA agonist, was blocked neither by naloxone nor by CCK-8, supporting the notion that CCK-8 is an endogenous opioid antagonist rather thana universal anti-hypotension agent.展开更多
文摘AIM To study the antagonism of cholecystokinin octapeptide (CCK 8) against effect of morphine and its mechanism. METHODS The electrical and mechanical activities of rat duodenum in vitro were recorded simultaneously. RESULTS Acetylcholine (ACh) could increase the amplitude and the number of the spike potential (SPA and SPN) of rat duodenum in vitro , followed by the increase of the duodenal contraction amplitudes (CA), showing a positive correlation. Morphine, on the contrary, inhibited the potentiation of ACh, showing a negative correlation. CCK 8 could antagonize the effects of morphine, i.e. SPA and SPN were increased again, followed by the increase of CA. CCK A receptor antagonist Devazepide could reverse the antagonism of CCK 8 to the effect of morphine. CONCLUSION CCK 8 could antagonize the effect of morphine which inhibited the potentiation of ACh on the duodenal activities in vitro . The antagonistic effect of CCK 8 on morphine was mainly mediated by CCK A receptor.
基金Project supported by the National Natural Science Foundation of China
文摘Previous studies have shown that CCK-8 has distinct antiopioid effect in the central sites related with pain control and blood pressure control. The aim of this study was to explore the receptor mechanism by which CCK-8 antagonized the depressor effect of u-and k-opioid agonists, and to observe whether CCK-8 could antagonize the depressor effect induced by muscimol, a nonopioid substance. The results showed that (ⅰ) The antagonistic effect of CCK-8 on opioid-induced hypotension could be blocked by intrathecal (i.t.) administration of CCK-B antagonist L-365, 260 at nanogram doses, or by CCK-A antagonist devazepide at doses 20—40 times higher than L-365, 260, indicating that it was the CCK-B receptor which mediates the antiopioid effect. (ⅱ) The depressor effect induced by intrathecal muscimol, a GABA agonist, was blocked neither by naloxone nor by CCK-8, supporting the notion that CCK-8 is an endogenous opioid antagonist rather thana universal anti-hypotension agent.
