Pepsin Release by Prostaglandin E1 Analogue: A Potential Therapeutic Problem

Marc D. Basson; Karl A. Zucker; Thomas E. Adrian; Michael J. Zdon; Garth H. Ballantyne; Irvin M. Modlin

doi:10.1001/archsurg.1988.01400280037007

Pepsin Release by Prostaglandin E1 Analogue: A Potential Therapeutic Problem

Marc D. Basson, Karl A. Zucker, Thomas E. Adrian, Michael J. Zdon, Garth H. Ballantyne, Irvin M. Modlin

Research output: Contribution to journal › Article › peer-review

5 Citations (Scopus)

Abstract

Prostaglandins inhibit gastric acid secretion and are independently “cytoprotective” for gastric mucosa. They are currently under clinical investigation for the treatment of peptic ulcers. The effects of the prostaglandin E₁ analogue misoprostol on pepsinogen and acid secretion were tested in isolated rabbit gastric glands and enriched parietal cells. Pepsinogen concentrations were measured by iodine 125—labeled albumin digestion and acid secretion indirectly by carbon 14—tagged aminopyrine uptake. Misoprostol inhibited histamine-stimulated acid secretion in parietal cells with 50% inhibition at 10⁻⁹ mol/L and maximally (78% inhibition) at 10⁷ mol/L. In contrast, however, misoprostol strongly stimulated pepsinogen secretion by gastric glands with a halfmaximal effect at 10⁻⁸ mol/L and maximal stimulation of 227% at 10⁶ mol/L. It is possible that this release of pepsin could compromise the action of prostaglandins in promoting ulcer healing.

Original language	English
Pages (from-to)	431-433
Number of pages	3
Journal	Archives of Surgery
Volume	123
Issue number	4
DOIs	https://doi.org/10.1001/archsurg.1988.01400280037007
Publication status	Published - Apr 1988
Externally published	Yes

ASJC Scopus subject areas

Surgery

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title = "Pepsin Release by Prostaglandin E1 Analogue: A Potential Therapeutic Problem",

abstract = "Prostaglandins inhibit gastric acid secretion and are independently “cytoprotective” for gastric mucosa. They are currently under clinical investigation for the treatment of peptic ulcers. The effects of the prostaglandin E1 analogue misoprostol on pepsinogen and acid secretion were tested in isolated rabbit gastric glands and enriched parietal cells. Pepsinogen concentrations were measured by iodine 125—labeled albumin digestion and acid secretion indirectly by carbon 14—tagged aminopyrine uptake. Misoprostol inhibited histamine-stimulated acid secretion in parietal cells with 50% inhibition at 10−9 mol/L and maximally (78% inhibition) at 107 mol/L. In contrast, however, misoprostol strongly stimulated pepsinogen secretion by gastric glands with a halfmaximal effect at 10−8 mol/L and maximal stimulation of 227% at 106 mol/L. It is possible that this release of pepsin could compromise the action of prostaglandins in promoting ulcer healing.",

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T1 - Pepsin Release by Prostaglandin E1 Analogue

T2 - A Potential Therapeutic Problem

AU - Basson, Marc D.

AU - Zucker, Karl A.

AU - Adrian, Thomas E.

AU - Zdon, Michael J.

AU - Ballantyne, Garth H.

AU - Modlin, Irvin M.

PY - 1988/4

Y1 - 1988/4

N2 - Prostaglandins inhibit gastric acid secretion and are independently “cytoprotective” for gastric mucosa. They are currently under clinical investigation for the treatment of peptic ulcers. The effects of the prostaglandin E1 analogue misoprostol on pepsinogen and acid secretion were tested in isolated rabbit gastric glands and enriched parietal cells. Pepsinogen concentrations were measured by iodine 125—labeled albumin digestion and acid secretion indirectly by carbon 14—tagged aminopyrine uptake. Misoprostol inhibited histamine-stimulated acid secretion in parietal cells with 50% inhibition at 10−9 mol/L and maximally (78% inhibition) at 107 mol/L. In contrast, however, misoprostol strongly stimulated pepsinogen secretion by gastric glands with a halfmaximal effect at 10−8 mol/L and maximal stimulation of 227% at 106 mol/L. It is possible that this release of pepsin could compromise the action of prostaglandins in promoting ulcer healing.

AB - Prostaglandins inhibit gastric acid secretion and are independently “cytoprotective” for gastric mucosa. They are currently under clinical investigation for the treatment of peptic ulcers. The effects of the prostaglandin E1 analogue misoprostol on pepsinogen and acid secretion were tested in isolated rabbit gastric glands and enriched parietal cells. Pepsinogen concentrations were measured by iodine 125—labeled albumin digestion and acid secretion indirectly by carbon 14—tagged aminopyrine uptake. Misoprostol inhibited histamine-stimulated acid secretion in parietal cells with 50% inhibition at 10−9 mol/L and maximally (78% inhibition) at 107 mol/L. In contrast, however, misoprostol strongly stimulated pepsinogen secretion by gastric glands with a halfmaximal effect at 10−8 mol/L and maximal stimulation of 227% at 106 mol/L. It is possible that this release of pepsin could compromise the action of prostaglandins in promoting ulcer healing.

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Pepsin Release by Prostaglandin E1 Analogue: A Potential Therapeutic Problem

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