Colonic glycoprotein secretion and calmodulin-acceptor proteins in the reserpine-treated rat.
Colonic glycoprotein secretion and calmodulin-acceptor proteins in the reserpine-treated rat.
复制标题
利血平治疗大鼠的结肠糖蛋白分泌和钙调蛋白受体蛋白。
DOI：
10.1152/ajpgi.1985.248.1.g54
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Dedman,JR
中科院分区：
文献类型：
--
作者：
Brady,RC;KarnakyJr,KJ;Dedman,JR
对长期接受利血平治疗的大鼠与注射盐水的对照大鼠的放射性前体标记的结肠糖蛋白分泌率进行了检查。发现利血平处理的大鼠制备的外翻结肠囊分泌过多，其糖蛋白分泌的基础率比对照外翻囊高三倍。此外，对照组织中的糖蛋白分泌受到促分泌剂卡巴胆碱的刺激，并且这种刺激被10μM三氟拉嗪（钙调蛋白拮抗剂）阻止。相比之下，经利血平处理的组织对卡巴胆碱和三氟拉嗪的处理具有抵抗力。虽然通过放射免疫测定证明利血平处理和对照结肠粘膜含有相同水平的钙调蛋白，但利血平处理的组织被确定缺乏两种分子量分别为29和47千道尔顿的钙调蛋白受体蛋白。数据表明，利血平在结肠粘膜内引发这种囊性纤维化样糖蛋白分泌过多状态的机制导致钙调蛋白在调节该分泌过程中的功能丧失。我们推测，囊性纤维化中存在的生化缺陷也可能导致糖蛋白分泌调节中钙调蛋白功能的丧失。
The rate of radioactive precursor-labeled colonic glycoprotein secretion in chronically reserpine-treated versus saline-injected control rats was examined. Everted colonic sacs prepared from reserpine-treated rats were found to be hypersecretory, exhibiting a basal rate of glycoprotein secretion that was threefold higher than control everted sacs. Furthermore, glycoprotein secretion in control tissue was stimulated by the secretagogue carbachol, and this stimulation was precluded by 10 microM trifluoperazine, the calmodulin antagonist. Reserpine-treated tissue, in contrast, was refractory to treatment with carbachol as well as trifluoperazine. While reserpine-treated and control colonic mucosae were demonstrated to contain equivalent levels of calmodulin via radioimmunoassay, reserpine-treated tissue was determined to lack two calmodulin-acceptor proteins with molecular weights of 29 and 47 kilodaltons. The data suggest that the mechanism by which reserpine elicits this cystic fibrosislike, hypersecretory state of glycoprotein secretion within the colonic mucosa entails the loss of calmodulin function in the regulation of this secretory process. We speculate that the biochemical defect present in cystic fibrosis could also entail such a loss of calmodulin function in the regulation of glycoprotein secretion.