CA IONOPHORE-STIMULATED ION SECRETION IN RABBIT ILEAL MUCOSA - RELATION TO ACTIONS OF CYCLIC 3',5'-AMP AND CARBAMYLCHOLINE
CA IONOPHORE-STIMULATED ION SECRETION IN RABBIT ILEAL MUCOSA - RELATION TO ACTIONS OF CYCLIC 3',5'-AMP AND CARBAMYLCHOLINE
复制标题
DOI：
10.1007/bf01869947
复制
发表时间：
1977-01-01
影响因子：
2.4
通讯作者：
FIELD, M
中科院分区：
文献类型：
--
作者：
BOLTON, JE;FIELD, M
Ca离子载体A23187 [2-[(3. β .,9. α .,11. β .-三甲基]-8-（2-吡咯羧甲基）-1,7-二氧嘧啶[6.6]十一烷基-2. β]的加入。-5-甲基氨基苯并恶唑-4-羧酸](0.5 .mu。g/ml)，对脱皮家兔回肠黏膜浆膜侧离子转运产生的变化与环[c]AMP和茶碱产生的变化定性相同：短路电流和电阻增加，由于单向黏膜(m)到浆膜(s)的通量减少而净分泌Cl，由于(m)到(m)的通量增加，净分泌Na由于(m)到(s)的通量减少而净分泌。细胞内cAMP水平的测量显示与离子载体孵育后没有变化。从浆膜浴介质中去除Ca可降低A23187的作用，但不影响茶碱的作用。用锶代替钙从粘膜和浆膜洗浴介质中去除钙，完全消除了对A23187的p.d[电位差]反应。离子载体显然是通过增加钙流入上皮细胞而引起其分泌作用。氨甲酰胆碱和血清素[5-羟色胺]是已知对肠粘膜细胞内cAMP水平没有影响的分泌剂，它们依赖于细胞外钙来产生完全的电反应（尽管，至少在氨甲酰胆碱的情况下，锶可以替代钙）。促分泌物血管活性肠肽和前列腺素E1提高肠黏膜cAMP浓度，似乎不需要外源性Ca。Ca可能是肠离子和水分泌的细胞内介质，一些肠促分泌物可能作为钙离子载体。
Addition of the Ca ionophore, A23187 [2-[(3.beta.,9.alpha.,11.beta.-trimethyl)-8-(2-pyrrolecarboxymethyl)-1,7-dioxaspiro[6.6]undecyl-2.beta.-methyl]-5-methylaminobenzoxazole-4-carboxylic acid] (0.5 .mu.g/ml), to the serosal side of stripped rabbit ileal mucosa produced changes in ion transport qualitatively identical with those produced by cyclic[c]AMP and theophylline: an increase in short-circuit current and resistance, net secretion of Cl due both to a decrease in the unidirectional mucosa (m) to serosa (s) flux and an increase in the (s) to (m) flux and net secretion of Na due to a decrease in (m) to (s) flux. Measurements of intracellular cAMP level demonstrated no change following incubation with the ionophore. Removal of Ca from the serosal bathing medium diminished the effects of A23187 but did not impair the action of theophylline. Removal of Ca from both the mucosal and serosal bathing media by replacing it with Sr completely abolished the p.d. [potential difference] response to A23187. The ionophore apparently elicits its secretory actions by increasing Ca influx into the epithelial cells. Carbamylcholine and serotonin [5-hydroxytryptamine], secretagogues known to have no effect on intracellular cAMP level in intestinal mucosa, were dependent on extracellular Ca to produce their full electrical response (although, in the case of carbamylcholine at least, Sr can substitute for Ca). The secretagogues vasoactive intestinal peptide and prostaglandin E1, which raise cAMP concentration in intestinal mucosa, do not appear to require external Ca. Ca may be an intracellular mediator of intestinal ion and water secretion and some intestinal secretagogues may act as Ca ionophores.