EFFECT OF ENDOGENOUS OPIOIDS ON VAGALLY INDUCED RELEASE OF GASTRIN, SOMATOSTATIN AND BOMBESIN-LIKE IMMUNOREACTIVITY FROM THE PERFUSED RAT STOMACH

The aim of the present study was to evaluate the effect of the opiate receptor antagonist naloxone on vagally stimulated secretion of bombes in-like immunoreactivity (BLI), somatostatin and gastrin from the isol ated rat stomach, which was perfused via the celiac artery with Krebs- Ringer buffer. Vagal stimulation was performed for 10 min with 1 ms, 1 0 V and 2, 5, 10 or 20 Hz, respectively. In control experiments BLI re lease increased significantly above basal secretion during a stimulati on frequency of 10 Hz (1367 +/- 357 pg/10 min; P < 0.001) and 20 Hz (9 96 +/- 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 secreti on 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), respe ctively. At 2 Hz naloxone had no effect on BLI release. As shown previ ously the cholinergic blocker atropine (10(-7) M) induced a significan t 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 c ombination of naloxone and atropine were similar to naloxone and atrop ine alone. Naloxone had no effect on vagal or GRP-induced regulation o f gastrin and somatostatin release. In conclusion, the present data de monstrate that endogenous opioids contribute to vagal regulation of BL I secretion. Stimulatory or inhibitory actions of endogenous opioids d epend on the stimulation frequency employed. Further studies in isolat ed nerve endings are required to discriminate direct from indirect act ions of endogenous opioids on the BLI neurons.