Cholecystokinin, carbachol, gastrin, histamine, and forskolin increase [Ca2+]i in gastric glands.
Cholecystokinin, carbachol, gastrin, histamine, and forskolin increase [Ca2+]i in gastric glands.
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胆囊收缩素、卡巴胆碱、胃泌素、组胺和毛喉素会增加胃腺中的[Ca2]i。
DOI：
10.1152/ajpgi.1986.250.6.g814
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Chew,CS
中科院分区：
文献类型：
--
作者：
Chew,CS
用钙离子选择性荧光探针Quin-2测定兔离体胃腺体内游离钙离子浓度的变化。卡巴胆碱和八肽缩胆囊素(CCK-8)均可使细胞内钙离子浓度[(Ca~(2+)]_i)一过性升高，最大升幅约为0.15~0.5微米，最大值出现在促分泌剂作用后的4-6个S内。[Ca~(2+)]i的升高呈剂量依赖性，并可被适当的拮抗剂抑制。用卡巴胆碱或CCK-8预刺激可有效地阻止另一种激动剂引起的[Ca~(2+)]i升高。细胞外钙离子的急性去除略微减少了在促分泌剂添加后的[钙]i增加，但对胃蛋白酶原的分泌没有影响。严重的钙耗竭导致Quin 2信号的强烈抑制和基础胃蛋白酶原释放的抑制，并减少但不是完全阻断对卡巴胆碱和CCK-8的胃蛋白酶原释放。胃泌素刺激也提高了腺体内的[Ca~(2+)]i，但这种激动剂的作用仅为CCK-8的40-50%。CAMP依赖的激动剂组胺和Forsklin增加[Ca~(2+)]i的程度与胃泌素大致相同。与卡巴胆碱和CCK-8相比，组胺和Forsklin模拟后[Ca~(2+)]i的升高有一定的滞后，这表明在激动剂-受体结合和用cAMP依赖的激动剂观察到的[Ca~(2+)]i升高之间发生了额外的生化事件。CAMP依赖和非依赖激动剂均可诱导自发荧光增强，其速度慢于[Ca~(2+)]i的升高，但同样受细胞外Ca~(2+)耗竭的影响。
The Ca2+-selective fluorescent probe quin 2 was used to measure changes in the concentration of free cytosolic [Ca2+] in isolated rabbit gastric glands. Both carbachol and cholecystokinin octapeptide (CCK-8) were found to increase transiently intracellular Ca2+ concentration, [( Ca2+]i) with maximal increases from approximately 0.15 to 0.5 microM occurring within 4–6 s following secretagogue addition. Increases in [Ca2+]i were dose dependent and inhibited by appropriate antagonists. Prestimulation with either carbachol or CCK-8 effectively prevented increases in [Ca2+]i in response to the other agonist. Acute removal of extracellular Ca2+ slightly reduced the increase in [Ca2+]i that occurred following secretagogue addition but had no effect on pepsinogen secretion. Severe Ca2+ depletion resulted in potent inhibition of the quin 2 signal and suppressed basal pepsinogen release and reduced, but did not totally block, pepsinogen release in response to carbachol and CCK-8. Gastrin stimulation also elevated [Ca2+]i in glands, but this agonist was only 40–50% as effective as CCK-8. The cAMP-dependent agonists histamine and forskolin increased [Ca2+]i to approximately the same degree as gastrin. There was a definite lag in the rise in [Ca2+]i following simulation with histamine and forskolin compared with carbachol and CCK-8, which suggests that additional biochemical events occur between agonist-receptor binding and the rise in [Ca2+]i observed with the cAMP-dependent agonists. Both cAMP-dependent and -independent agonists induced an increase in autofluorescence that was slower than the rise in [Ca2+]i but equally affected by extracellular Ca2+ depletion.