Insulin, glucagon and somatostatin in the perfused rat pancreas and the effects of HB 699 (4-(2-(5-chloro-2-metoxy-benzamido)-ethyl)-benzoic acid).

HB 699 (100 micrograms/ml), almost identical with the left residue of the sulphonylurea glibenclamide, enhanced basal insulin and somatostatin release from the perfused rat pancreas. The compound also augmented both the early and late insulin release stimulated by 6.7 mM glucose, while with 16.7 and 33.3 mM glucose only late insulin release was increased. Furthermore, HB 699 enhanced both phases of glucose induced somatostatin release irrespective of whether 6.7, 16.7 or 33.3 mM glucose were used. As for glucagon release, HB 699 suppressed basal and arginine stimulated glucagon secretion. The present findings imply that the sulphonylurea moiety of glibenclamide is not a prerequisite for its stimulatory action on insulin and somatostatin release. It is suggested that the enhanced somatostatin release mediates the inhibitory effect of the compound on glucagon release.