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Physiological significance of ECL-cell histamine.
In the oxyntic mucosa of the mammalian stomach, histamine is stored in ECL cells and in mucosal mast cells. In the rat, at least 80 percent of oxyntic mucosal histamine resides in the ECL cells. Histamine is a key factor in the regulation of gastric acid secretion. Following depletion of ECL-cell hi...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Yale Journal of Biology and Medicine
1998
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2578996/ https://www.ncbi.nlm.nih.gov/pubmed/10461351 |
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author | Andersson, K. Chen, D. Mattsson, H. Sundler, F. Håkanson, R. |
author_facet | Andersson, K. Chen, D. Mattsson, H. Sundler, F. Håkanson, R. |
author_sort | Andersson, K. |
collection | PubMed |
description | In the oxyntic mucosa of the mammalian stomach, histamine is stored in ECL cells and in mucosal mast cells. In the rat, at least 80 percent of oxyntic mucosal histamine resides in the ECL cells. Histamine is a key factor in the regulation of gastric acid secretion. Following depletion of ECL-cell histamine by treatment with alpha-fluoromethylhistidine (alpha-FMH), basal acid secretion was reduced, and gastrin-stimulated acid secretion was abolished. Vagally-induced acid secretion (by insulin injection or pylorus ligation) was unaffected by alpha-FMH treatment but inhibited by an H2 antagonist. These results suggest that gastrin stimulates acid secretion via release of ECL-cell histamine, whereas vagally-induced acid secretion--although histamine-dependent--does not rely on ECL-cell histamine. Gastrin is known to have a trophic effect on the oxyntic mucosa. By combining long-term hypergastrinemia with continuous infusion of alpha-FMH, we were able to show that gastrin-evoked trophic effects in the stomach do not depend on ECL-cell histamine. |
format | Text |
id | pubmed-2578996 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1998 |
publisher | Yale Journal of Biology and Medicine |
record_format | MEDLINE/PubMed |
spelling | pubmed-25789962008-11-05 Physiological significance of ECL-cell histamine. Andersson, K. Chen, D. Mattsson, H. Sundler, F. Håkanson, R. Yale J Biol Med Research Article In the oxyntic mucosa of the mammalian stomach, histamine is stored in ECL cells and in mucosal mast cells. In the rat, at least 80 percent of oxyntic mucosal histamine resides in the ECL cells. Histamine is a key factor in the regulation of gastric acid secretion. Following depletion of ECL-cell histamine by treatment with alpha-fluoromethylhistidine (alpha-FMH), basal acid secretion was reduced, and gastrin-stimulated acid secretion was abolished. Vagally-induced acid secretion (by insulin injection or pylorus ligation) was unaffected by alpha-FMH treatment but inhibited by an H2 antagonist. These results suggest that gastrin stimulates acid secretion via release of ECL-cell histamine, whereas vagally-induced acid secretion--although histamine-dependent--does not rely on ECL-cell histamine. Gastrin is known to have a trophic effect on the oxyntic mucosa. By combining long-term hypergastrinemia with continuous infusion of alpha-FMH, we were able to show that gastrin-evoked trophic effects in the stomach do not depend on ECL-cell histamine. Yale Journal of Biology and Medicine 1998 /pmc/articles/PMC2578996/ /pubmed/10461351 Text en |
spellingShingle | Research Article Andersson, K. Chen, D. Mattsson, H. Sundler, F. Håkanson, R. Physiological significance of ECL-cell histamine. |
title | Physiological significance of ECL-cell histamine. |
title_full | Physiological significance of ECL-cell histamine. |
title_fullStr | Physiological significance of ECL-cell histamine. |
title_full_unstemmed | Physiological significance of ECL-cell histamine. |
title_short | Physiological significance of ECL-cell histamine. |
title_sort | physiological significance of ecl-cell histamine. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2578996/ https://www.ncbi.nlm.nih.gov/pubmed/10461351 |
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