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  • Title: Actions of neuromedin-B and neuromedin-C on amylase release from isolated rat pancreatic acini.
    Author: Otsuki M, Fujii M, Nakamura T, Tani S, Oka T, Baba S, Yajima H.
    Journal: Pancreas; 1987; 2(3):252-7. PubMed ID: 2442745.
    Abstract:
    Neuromedin-B and neuromedin-C are novel decapeptides which have recently been isolated from porcine spinal cord and canine intestinal muscle, and show striking sequence homology with gastrin-releasing peptide (GRP-27) at the carboxyl-terminal region. The effects of synthetic neuromedin-B and neuromedin-C on exocrine pancreatic function were examined using isolated rat pancreatic acini. Neuromedin-B and neuromedin-C were able to cause full stimulation of amylase release. The relative efficacy of neuromedin-B and neuromedin-C was the same as that of GRP-27. Neuromedin-C was about twofold more potent, whereas, neuromedin-B was about 10-fold less potent than GRP-27. Both neuromedin-B and neuromedin-C potentiated the stimulation of amylase release caused by vasoactive intestinal peptide, secretin, or forskolin. Potentiation of amylase secretion did not occur with neuromedin-B or neuromedin-C plus cholecystokinin (CCK), carbamylcholine, or Ca2+ ionophore A23187. The effects of neuromedin-B and neuromedin-C on enzyme secretion were inhibited neither by dibutyryl cyclic GMP, nor atropine. The present study suggests that neuromedin-B and neuromedin-C act on different receptors than CCK and cholinergic agents, but appear to activate a common intracellular mechanism.
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