ROLE OF CALCIUM IN THE BOMBESIN-INDUCED INTESTINAL CCK RELEASE IN RATS

In the isolated vascularly perfused rat duodenojejunum, vascular infus ion of bombesin (100 nM) provoked an early, transient (6 min) release of CCK (500% of basal), followed by a sustained response (400% of basa l). The calcium chelator EGTA (2 mM) reduced the early peak and abolis hed the second phase of CCK release. A similar variation was evoked by verapamil (10 muM), whereas diltiazem (100 muM), nifedipine (50 muM), and omega-conotoxin (100 nM) had no significant effect. It is conclud ed that bombesin-induced CCK release from rat intestine is dependent o n the availability of extracellular calcium and on the activation of c alcium channels sensitive to blockers of the phenylalkylamine family.