Gastrin receptors on isolated canine parietal cells.
Gastrin receptors on isolated canine parietal cells.
复制标题
分离的犬壁细胞上的胃泌素受体。
DOI：
10.1172/jci111348
复制
发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Elashoff,JD
中科院分区：
文献类型：
--
作者：
Soll,AH;Amirian,DA;Thomas,LP;Reedy,TJ;Elashoff,JD
已经研究了胃底粘膜中介导胃泌素刺激酸分泌的受体。合成的人胃泌素-17-I（G17）在第15位（[Leu 15]-G17）有亮氨酸取代，用氯胺T碘化;发现与酶分散的犬胃底粘膜细胞有高饱和结合。127 I-[Leu 15]-G17，而不是127 I-G17，保留了与单碘化G17相当的结合效力和生物活性。通过使用淘析器转子按大小分离胃底粘膜细胞，并且较大细胞组分中的特异性125 I-[Leu-15]-G17结合与壁细胞的分布高度相关。然而，有特定的胃泌素结合在小细胞组分，不占壁细胞。使用连续淘洗和逐步密度梯度，高度富集壁细胞和主细胞组分制备; 125 I-[Leu 15]-G17结合与壁细胞呈正相关（r = 0.98），与主细胞含量呈负相关（r = -0.96）。在富含45-65%壁细胞的组分中，特异性125 I-[Leu 15]-G17结合迅速，在37 ℃下30分钟内达到稳定状态。解离也迅速，在100倍稀释或稀释加过量五肽胃泌素后的速率相似。在示踪剂浓度为10 - 30 pM时，饱和结合为7.8 +/- 0.8%/10（6）个细胞（平均值+/- SE），在过量五肽胃泌素存在下的结合占总结合的11%。G17和胆囊收缩素的羧基末端八肽（26-33）在取代示踪剂结合和刺激壁细胞功能（[14 C]氨基比林积累）方面是等效的，而胃泌素的四肽（14-17）的效力要低得多。丙谷胺抑制胃泌素结合，并选择性抑制胃泌素刺激壁细胞功能。犬的壁细胞具有特异性胃泌素受体，介导壁细胞功能的刺激。胃泌素受体在主细胞上检测不到，但存在于另一个较小的粘膜细胞上。
The receptors in the fundic mucosa that mediate gastrin stimulation of acid secretion have been studied. Synthetic human gastrin-17-I (G17) with a leucine substitution in the 15th position ( [Leu15]-G17) was iodinated by chloramine T; high saturable binding was found to enzyme-dispersed canine fundic mucosal cells. 127I-[Leu15]-G17, but not 127I-G17, retained binding potency and biological activity comparable with uniodinated G17. Fundic mucosal cells were separated by size by using an elutriator rotor, and specific 125I-[Leu-15]-G17 binding in the larger cell fractions was highly correlated with the distribution of parietal cells. There was, however, specific gastrin binding in the small cell fractions, not accounted for by parietal cells. Using sequential elutriation and stepwise density gradients, highly enriched parietal and chief cell fractions were prepared; 125I-[Leu15]-G17 binding correlated positively with the parietal cell (r = 0.98) and negatively with chief cell content (r = -0.96). In fractions enriched to 45-65% parietal cells, specific 125I-[Leu15]-G17 binding was rapid, reaching a steady state at 37 degrees C within 30 min. Dissociation was also rapid, with the rate similar after 100-fold dilution or dilution plus excess pentagastrin. At a tracer concentration from 10 to 30 pM, saturable binding was 7.8 +/- 0.8% per 10(6) cells (mean +/- SE) and binding in the presence of excess pentagastrin accounted for 11% of total binding. G17 and carboxyl terminal octapeptide of cholecystokinin (26-33) were equipotent in displacing tracer binding and in stimulating parietal cell function ( [14C]aminopyrine accumulation), whereas the tetrapeptide of gastrin (14-17) had a much lower potency. Proglumide inhibited gastrin binding and selectively inhibited gastrin stimulation of parietal cell function. Canine parietal cells have specific receptors for gastrin that mediate stimulation of parietal cell function. Gastrin receptors were undetectable on chief cells, and yet present on another smaller mucosal cell(s).