author_facet Nishida, A.
Kobayashi-Uchida, A.
Akuzawa, S.
Takinami, Y.
Shishido, T.
Kamato, T.
Ito, H.
Yamano, M.
Yuki, H.
Nagakura, Y.
et, al.
Nishida, A.
Kobayashi-Uchida, A.
Akuzawa, S.
Takinami, Y.
Shishido, T.
Kamato, T.
Ito, H.
Yamano, M.
Yuki, H.
Nagakura, Y.
et, al.
author Nishida, A.
Kobayashi-Uchida, A.
Akuzawa, S.
Takinami, Y.
Shishido, T.
Kamato, T.
Ito, H.
Yamano, M.
Yuki, H.
Nagakura, Y.
et, al.
spellingShingle Nishida, A.
Kobayashi-Uchida, A.
Akuzawa, S.
Takinami, Y.
Shishido, T.
Kamato, T.
Ito, H.
Yamano, M.
Yuki, H.
Nagakura, Y.
et, al.
American Journal of Physiology-Gastrointestinal and Liver Physiology
Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
Physiology (medical)
Gastroenterology
Hepatology
Physiology
author_sort nishida, a.
spelling Nishida, A. Kobayashi-Uchida, A. Akuzawa, S. Takinami, Y. Shishido, T. Kamato, T. Ito, H. Yamano, M. Yuki, H. Nagakura, Y. et, al. 0193-1857 1522-1547 American Physiological Society Physiology (medical) Gastroenterology Hepatology Physiology http://dx.doi.org/10.1152/ajpgi.1995.269.5.g699 <jats:p> Female rats were treated orally for 13 wk with YM022 (300 mumol.kg-1.day-1) and with omeprazole (400 mumol.kg-1.day-1) or famotidine (900 mumol.kg-1.day-1) with or without YM022. At 2 h after the last dose, YM022 and omeprazole markedly inhibited basal and pentagastrin-induced acid secretion. Famotidine was less potent than YM022 and omeprazole against both secretions. The degree of increase in plasma gastrin level in the three groups was parallel to the antisecretory potencies of the drugs. At 14 days after the cessation of omeprazole treatment, the secretory response to pentagastrin increased above that of the control. This hyperresponse lasted for &gt; or = 56 days. In the famotidine-treated group, a small increase in secretory response to pentagastrin was observed but was not statistically significant. The increase in secretory response to pentagastrin was paralleled by an increase in mucosal cell mass. In contrast, YM022 not only exhibited a long-lasting inhibition of pentagastrin-induced acid secretion but also prevented the hyperresponse to pentagastrin caused by omeprazole. These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats. </jats:p> Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression American Journal of Physiology-Gastrointestinal and Liver Physiology
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series American Journal of Physiology-Gastrointestinal and Liver Physiology
source_id 49
title Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_unstemmed Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_full Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_fullStr Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_full_unstemmed Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_short Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_sort gastrin receptor antagonist ym022 prevents hypersecretion after long-term acid suppression
topic Physiology (medical)
Gastroenterology
Hepatology
Physiology
url http://dx.doi.org/10.1152/ajpgi.1995.269.5.g699
publishDate 1995
physical G699-G705
description <jats:p> Female rats were treated orally for 13 wk with YM022 (300 mumol.kg-1.day-1) and with omeprazole (400 mumol.kg-1.day-1) or famotidine (900 mumol.kg-1.day-1) with or without YM022. At 2 h after the last dose, YM022 and omeprazole markedly inhibited basal and pentagastrin-induced acid secretion. Famotidine was less potent than YM022 and omeprazole against both secretions. The degree of increase in plasma gastrin level in the three groups was parallel to the antisecretory potencies of the drugs. At 14 days after the cessation of omeprazole treatment, the secretory response to pentagastrin increased above that of the control. This hyperresponse lasted for &gt; or = 56 days. In the famotidine-treated group, a small increase in secretory response to pentagastrin was observed but was not statistically significant. The increase in secretory response to pentagastrin was paralleled by an increase in mucosal cell mass. In contrast, YM022 not only exhibited a long-lasting inhibition of pentagastrin-induced acid secretion but also prevented the hyperresponse to pentagastrin caused by omeprazole. These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats. </jats:p>
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author Nishida, A., Kobayashi-Uchida, A., Akuzawa, S., Takinami, Y., Shishido, T., Kamato, T., Ito, H., Yamano, M., Yuki, H., Nagakura, Y., et, al.
author_facet Nishida, A., Kobayashi-Uchida, A., Akuzawa, S., Takinami, Y., Shishido, T., Kamato, T., Ito, H., Yamano, M., Yuki, H., Nagakura, Y., et, al., Nishida, A., Kobayashi-Uchida, A., Akuzawa, S., Takinami, Y., Shishido, T., Kamato, T., Ito, H., Yamano, M., Yuki, H., Nagakura, Y., et, al.
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description <jats:p> Female rats were treated orally for 13 wk with YM022 (300 mumol.kg-1.day-1) and with omeprazole (400 mumol.kg-1.day-1) or famotidine (900 mumol.kg-1.day-1) with or without YM022. At 2 h after the last dose, YM022 and omeprazole markedly inhibited basal and pentagastrin-induced acid secretion. Famotidine was less potent than YM022 and omeprazole against both secretions. The degree of increase in plasma gastrin level in the three groups was parallel to the antisecretory potencies of the drugs. At 14 days after the cessation of omeprazole treatment, the secretory response to pentagastrin increased above that of the control. This hyperresponse lasted for &gt; or = 56 days. In the famotidine-treated group, a small increase in secretory response to pentagastrin was observed but was not statistically significant. The increase in secretory response to pentagastrin was paralleled by an increase in mucosal cell mass. In contrast, YM022 not only exhibited a long-lasting inhibition of pentagastrin-induced acid secretion but also prevented the hyperresponse to pentagastrin caused by omeprazole. These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats. </jats:p>
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spelling Nishida, A. Kobayashi-Uchida, A. Akuzawa, S. Takinami, Y. Shishido, T. Kamato, T. Ito, H. Yamano, M. Yuki, H. Nagakura, Y. et, al. 0193-1857 1522-1547 American Physiological Society Physiology (medical) Gastroenterology Hepatology Physiology http://dx.doi.org/10.1152/ajpgi.1995.269.5.g699 <jats:p> Female rats were treated orally for 13 wk with YM022 (300 mumol.kg-1.day-1) and with omeprazole (400 mumol.kg-1.day-1) or famotidine (900 mumol.kg-1.day-1) with or without YM022. At 2 h after the last dose, YM022 and omeprazole markedly inhibited basal and pentagastrin-induced acid secretion. Famotidine was less potent than YM022 and omeprazole against both secretions. The degree of increase in plasma gastrin level in the three groups was parallel to the antisecretory potencies of the drugs. At 14 days after the cessation of omeprazole treatment, the secretory response to pentagastrin increased above that of the control. This hyperresponse lasted for &gt; or = 56 days. In the famotidine-treated group, a small increase in secretory response to pentagastrin was observed but was not statistically significant. The increase in secretory response to pentagastrin was paralleled by an increase in mucosal cell mass. In contrast, YM022 not only exhibited a long-lasting inhibition of pentagastrin-induced acid secretion but also prevented the hyperresponse to pentagastrin caused by omeprazole. These results indicate that the hypergastrinemia caused by long-term administration of antisecretory drugs increases mucosal secretory response to pentagastrin through a gastrin/cholecystokinin B receptor-mediated pathway in rats. </jats:p> Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression American Journal of Physiology-Gastrointestinal and Liver Physiology
spellingShingle Nishida, A., Kobayashi-Uchida, A., Akuzawa, S., Takinami, Y., Shishido, T., Kamato, T., Ito, H., Yamano, M., Yuki, H., Nagakura, Y., et, al., American Journal of Physiology-Gastrointestinal and Liver Physiology, Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression, Physiology (medical), Gastroenterology, Hepatology, Physiology
title Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_full Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_fullStr Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_full_unstemmed Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_short Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
title_sort gastrin receptor antagonist ym022 prevents hypersecretion after long-term acid suppression
title_unstemmed Gastrin receptor antagonist YM022 prevents hypersecretion after long-term acid suppression
topic Physiology (medical), Gastroenterology, Hepatology, Physiology
url http://dx.doi.org/10.1152/ajpgi.1995.269.5.g699