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The roles of pepsinogen and agmatine in normal human gastric acid production and tissue protection

Author Howard W. Steer
Institution Southampton General Hospital,
Southampton University Hospitals NHS Trust,
University of Southampton School of Medicine,
Southampton, SO16 6YD United Kingdom.
Copyright © Howard Steer 2007.

All rights reserved. This publication is copyright under the Berne Convention and the International Copyright Convention. No part of this publication may be reproduced, stored in a retrieval system or transmitted, in any form or by any means without the prior permission of the copyright holder. Enquires concerning reproduction outside the scope of the above should be sent to: mail@howardsteer.co.uk.

Abstract

The production of concentrated acid by the human stomach with the absence of any harmful effects of this concentrated acid on the normal stomach has lacked satisfactory explanation. Evidence is presented for the decarboxylation of the basic amino acid arginine being involved in this process. The arginine is derived from the activation segment of pepsinogens. The decarboxylation of arginine is extracellular and occurs in the parietal cell canaliculi. The production of gastric acid by the hydration of this carbon dioxide is extracellular and occurs in the parietal cell canaliculi. Agmatine, which is formed by the decarboxylation of arginine, contributes to the defence of the tissues against the concentrated acid. This mechanism of acid production provides a satisfactory explanation as to why normal gastric acid production does not have an adverse effect on gastric tissues.

Keywords:  Pepsinogen, arginine, agmatine, gastric acid.



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