The release of rat intestinal cholecystokinin after oral trypsin inhibitor measured by bio‐assay.

The release of rat intestinal cholecystokinin after oral trypsin inhibitor measured by bio‐assay.
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生物测定法测定口服胰蛋白酶抑制剂后大鼠肠道缩胆囊素的释放。

DOI:
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发表时间:
1981
期刊:
Journal of Physiology
影响因子:
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通讯作者:
R. G. Morgan
R. G. Morgan
中科院分区:
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文献类型:
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作者:
S. Brand;R. G. Morgan

文献摘要

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采用体外胆囊生物测定法研究了大鼠小肠提取物中胆囊收缩素(CCK)样活性的分布、分子形态和释放。与报道的肠道CCK样免疫反应的异质性相反,使用生物测定法仅检测到单一分子形式的CCK样活性。2. 从Sephadex G50中洗脱的CCK - like活性(Kav为0.69),在胆囊收缩素三acontriepin (CCK33)之后,在胆囊收缩素八肽2500之前,可能代表CCK的22个氨基酸肽(CCK22)。CCK样活性的生物测定峰具有胰酶活性和CCK/胃泌素C末端免疫反应性。在中性pH条件下,很容易从小肠中提取出CCK样活性,但随后用0.5 M醋酸冷处理,进一步提取出与中性条件下相同的分子形式的CCK样活性。3. 对大鼠肠道提取物进行Sephadex G50层析后,该生物测定法未检测到CCK样活性,也未在CCK33或CCK8对应的组分中发现胰酶样活性。4. 口服胰蛋白酶抑制剂能有效刺激大鼠上小肠释放CCK样活性。口服胰蛋白酶抑制剂释放后,CCK‐样活性迅速重新合成。
The distribution, molecular form and release of cholecystokinin (CCK)‐like activity in extracts of rat small intestine was studied with an in vitro gall‐bladder bio‐assay. In contrast to the reported heterogeneity of CCK‐like immunoreactivity in the intestine, only a single molecular form of CCK‐like activity was detected using the bio‐assay. 2. The CCK‐like activity eluted from Sephadex G50 with a Kav of 0.69, after the triacontriapeptide of cholecystokinin (CCK33) and before cholecystokinin octapeptide 2500, may represent the 22 amino acid peptide of CCK (CCK22). The bio‐assay peak of CCK‐like activity had pancreozymin activity and CCK/gastrin C terminal immunoreactivity. The CCK‐like activity weas readily extracted from the small intestine at neutral pH, but subsequent treatment with cold 0.5 M‐acetic acid extracted further CCK‐like activity of the same molecular form as that recovered under neutral conditions. 3. The bio‐assay detected no CCK‐like activity, nor was pancreozymin‐like activity found in fractions corresponding to CCK33 or CCK8 after Sephadex G50 chromatography of rat intestinal extracts. 4. Oral trypsin inhibitor was a potent stimulus for the release of CCK‐like activity from the upper small intestine of the rat. After oral trypsin inhibitor release, CCK‐like activity was rapidly resynthesized.