Proglumide, a putative gastrin receptor antagonist, inhibited cholecystokinin (CCK)-stimulated amylase release and [3H]-2-deoxy-D-glucose uptake by isolated mouse pancreatic acini. Inhibition was reversible and competitive in nature with a KIof 0.7 mM. Proglumide also competitively inhibited the binding of 125I-CCK to its receptor in pancreas and brain; the KI for this interaction was 1.0 mM. In contrast, proglumide did not inhibit carbachol-stimulated amylase release, insulin-stimulated glucose transport and protein synthesis, or the binding of insulin to its receptors. Proglumide at 10 mM did, however, reduce both basal [3H]-2-deoxy-D-glucose uptake and [3H]-leucine incorporation into protein. We conclude that proglumide is a competitive and specific, albeit weak antagonist of CCK receptors. Higher concentrations of the drug may have other more nonspecific effects.

Journal Section:
Original Paper
Keywords:
Pancreas, Proglumide, Cholecystokinin, Amylase, Pancreatic secretion, Acetylcholine, Insulin
This content is only available via PDF.
© 1983 S. Karger AG, Basel
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
1983
You do not currently have access to this content.