Effect of endogenous opioids on vagally induced release of gastrin, somatostatin and bombesin-like immunoreactivity from the perfused rat stomach

Abstract

The aim of the present study was to evaluate the effect of the opiate receptor antagonist naloxone on vagally stimulated secretion of bombesin-like immunoreactivity (BLI), somatostatin and gastrin from the isolated rat stomach, which was perfused via the celiac artery with Krebs-Ringer buffer. Vagal stimulation was performed for 10 min with 1 ms, 10 V and 2, 5, 10 or 20 Hz, respectively. In control experiments BLI release increased significantly above basal secretion during a stimulation frequency of 10 Hz (1367 ± 357 pg/10 min; P < 0.001) and 20 Hz (996 ± 202 pg/10 min; P < 0.01), but not at 2 and 5 Hz. In comparison to the controls naloxone (10 −6 M) significantly increased BLI secretion at 5 Hz by 573 ± 150 pg/10 min ( P < 0.05), but attenuated the BLI response to higher stimulation frequencies of 10 and 20 Hz to 284 ± 143 pg/10 min ( P < 0.001) and 490 ± 114 pg/10 min ( P < 0.01), respectively. At 2 Hz naloxone had no effect on BLI release. As shown previously the cholinergic blocker atropine (10 −7 M) induced a significant BLI release during vagal stimulation at 2 Hz (680 ± 233 pg/10 min; P < 0.01) and 5 Hz (935 ± 324 pg/10 min; P < 0.05), but was without effect at 10 and 20 Hz compared to the controls. The effects of the combination of naloxone and atropine were similar to naloxone and atropine alone. Naloxone had no effect on vagal or GRP-induced regulation of gastrin and somatostatin release. In conclusion, the present data demonstrate that endogenous opioids contribute to vagal regulation of BLI secretion. Stimulatory or inhibitory actions of endogenous opioids depend on the stimulation frequency employed. Further studies in isolated nerve endings are required to discriminate direct from indirect actions of endogenous opioids on the BLI neurons.