Specific inhibition by prostaglandins E2 and I2 of histamine-stimulated [14C]aminopyrine accumulation and cyclic adenosine monophosphate generation by isolated canine parietal cells.
Specific inhibition by prostaglandins E2 and I2 of histamine-stimulated [14C]aminopyrine accumulation and cyclic adenosine monophosphate generation by isolated canine parietal cells.
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前列腺素 E2 和 I2 对组胺刺激的[14C]氨基比林积累和分离的犬壁细胞的环磷酸腺苷产生的特异性抑制。
DOI：
10.1172/jci109777
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
A. Soll
中科院分区：
文献类型：
--
作者：
A. Soll
本文研究了前列腺素E_2和I_2对壁细胞含量丰富的分散的犬胃粘膜细胞积聚[14C]氨基比林和产生环腺苷酸的影响。使用淋洗器转子将组分的壁细胞含量浓缩到43%至70%之间。以[14C]氨基比林蓄积量作为壁细胞对刺激反应的指标。前列腺素E2(PGE2，0.1 NM-0.1 mM)可抑制组胺刺激的氨基比林摄取，但不能阻断卡巴胆碱、胃泌素或二丁基环AMP的反应。然而，当对氨基比林和胃泌素的反应被组胺增强时，PGE2确实抑制了氨基比林的摄取。PGE2(0.1 nM-0.1 mM)以剂量依赖的方式抑制组胺刺激的环磷酸腺苷的产生，在1微米PGE2时抑制作用最大。前列环素还抑制组胺刺激的氨基比林蓄积和组胺刺激的环磷酸腺苷的产生。在没有添加组胺的情况下，浓度高于1微米的前列腺素E_2和浓度高于10微米的前列环素可能通过作用于非壁细胞来刺激环磷酸腺苷的产生，如先前的研究所表明的那样。这些目前的数据与前列腺素E2和I2通过特异性阻断组胺刺激的环状AMP产生来抑制分离的壁细胞对组胺的反应的假设是一致的。
The effects of prostaglandins E2 and I2 on accumulation of [14C]aminopyrine and the generation of cyclic AMP by fractions of dispersed canine gastric mucosal cells, enriched in their content of parietal cells, have been studied. The parietal cell content of the fractions was enriched to between 43 and 70% using an elutriator rotor. The accumulation of [14C]aminopyrine was used as the index of parietal cell response to stimulation. Prostaglandin E2 (PGE2, 0.1 nM-0.1 mM) inhibited histamine stimulated aminopyrine uptake but did not block the response to carbachol, gastrin, or dibuturyl cyclic AMP. PGE2 did, however, inhibit aminopyrine uptake stimulated by carbachol and gastrin when the response to these agents was potentiated by histamine. PGE2 (0.1 NM-0.1 mM) inhibited histamine-stimulated cyclic AMP production in a dose-dependent fashion with maximal inhibition at 1 microM PGE2. Prostacyclin also inhibited both histamine-stimulated aminopyrine accumulation and histamine-stimulated cyclic AMP production. In the absence of added histamine, PGE2 in concentrations above 1 microM and prostacyclin in concentrations above 10 microM stimulated cyclic AMP production, probably by acting on the nonparietal cells as shown in previous studies. These present data are consistent with the hypothesis that prostaglandins E2 and I2 inhibit the response of isolated parietal cells to histamine by specifically blocking histamine-stimulated cyclic AMP production.