Direct effects of nitric oxide on histamine release from rat enterochromaffin-like cells.
Direct effects of nitric oxide on histamine release from rat enterochromaffin-like cells.
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DOI：
10.1016/j.ejphar.2006.01.058
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发表时间：
2006-03
影响因子：
5
通讯作者：
Naozumi Shibata;H. Matsui;T. Yokota;B. Matsuura;K. Maeyama;M. Onji
中科院分区：
文献类型：
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作者：
Naozumi Shibata;H. Matsui;T. Yokota;B. Matsuura;K. Maeyama;M. Onji
一氧化氮（NO）对肠嗜铬样（ECL）细胞的直接作用尚未得到证实。在这项研究中，我们研究了NO供体对大鼠ECL细胞的直接影响。NO供体NOR3（10和100μM）减少胃泌素诱导的组胺释放。100μM NOR3增加cGMP水平并减少胃泌素诱导的钙内流。鸟苷酸环化酶抑制剂ODQ完全阻断NOR 3诱导的组胺释放抑制作用。这些结果表明，NO抑制胃酸分泌，通过抑制胃泌素诱导的组胺释放的途径，其中NO激活鸟苷酸环化酶，除了增加cGMP水平和减少胃泌素诱导的钙内流。使用NO作为降低胃中组胺水平的新型胃酸抑制剂将是有益的，因为使用组胺H2受体拮抗剂或质子泵抑制剂导致的组胺水平增加对肿瘤和免疫功能具有各种影响。
The direct effects of nitric oxide (NO) on enterochromaffin-like (ECL) cells have not yet been demonstrated. In this study we investigated the direct effects of NO donors on rat ECL cells. The NO donor, NOR3 (10 and 100μM), decreased gastrin-induced histamine release. 100μM NOR3 increased cGMP levels and reduced gastrin-induced calcium influx. ODQ, an inhibitor of guanylate cyclase, completely blocked NOR3-induced inhibition of histamine release. These results suggest that NO inhibits gastric acid secretion via suppression of gastrin-induced histamine release through a pathway in which NO activates guanylate cyclase, in addition to increasing cGMP levels and reducing gastrin-induced calcium influx. The use of NO as a new type of gastric acid inhibitor that decreases histamine levels in the stomach would be beneficial as increased histamine levels resulting from use of a histamine H2receptor antagonist or proton pump inhibitor have various effects on tumors and immunological functions.