Relationship between hormonal activation of phosphatidylinositol hydrolysis, fluid secretion and calcium flux in the blowfly salivary gland.
Relationship between hormonal activation of phosphatidylinositol hydrolysis, fluid secretion and calcium flux in the blowfly salivary gland.
复制标题
苍蝇唾液腺中磷脂酰肌醇水解、液体分泌和钙通量的激素激活之间的关系。
作者：
J. Fain;M. Berridge
另外，5-羟色胺刺激的流体分泌，跨上皮钙转运和分解的32 P-或3 H-标记的磷脂酰肌醇的分解[32 P]磷脂酰胆碱和[32 P]-磷脂酰乙醇胺没有被5-羟色胺刺激。在与肌-[2- 3 H]肌醇孵育1- 3小时的唾液腺中，超过95%的标记物以磷脂酰肌醇的形式保留在组织中。5-羟色胺的加入导致标记物在细胞内肌醇1：2-环磷酸、肌醇1-磷酸和游离肌醇中的积累增加沿着同时[3 H]肌醇向培养基和唾液的释放增加。[3 H]肌醇释放到培养基中作为磷脂酰肌醇分解的敏感指标。[3 H]肌醇的释放没有增加环AMP或二价阳离子离子载体A23187的条件下，唾液分泌加速。3-异丁基-1-甲基黄嘌呤可增强低浓度5-羟色胺对液体分泌的刺激作用，但对肌醇的释放无影响。在无钙缓冲液中，5-羟色胺对液体分泌的刺激大大减少，但在无钙的情况下，磷脂酰肌醇的分解仍以相同的速率继续。这些结果支持这一假设，即5-羟色胺的磷脂酰肌醇的分解参与钙的门控。
The addition of 5-hydroxytryptamine to the isolated blowfly salivary gland stimulates fluid secretion, transepithelial calcium transport and the breakdown of 32P- or 3H-labelled phosphatidylinositol The breakdown of [32P]phosphatidylcholine and [32P]-phosphatidylethanolamine was not stimulated by 5-hydroxytryptamine. In salivary glands incubated with myo-[2-3H]inositol for 1--3 h, more than 95% of the label retained by the tissue was in the form of phosphatidylinositol. The addition of 5-hydroxytryptamine resulted in an increase in the accumulation of label in intracellular inositol 1:2-cyclic phosphate, inositol 1-phosphate and free inositol along with an increase in the release of [3H]inositol to the medium and saliva. The release of [3H]inositol to the medium served as a sensitive indicator of phosphatidylinositol breakdown. The release of [3H]inositol was not increased by cyclic AMP or the bivalent-cation ionophore A23187 under conditions in which salivary secretion was accelerated. The stimulation of fluid secretion by low concentrations of 5-hydroxytryptamine was potentiated by 3-isobutyl-1-methylxanthine, which had no effect on inositol release. The stimulation of fluid secretion by 5-hydroxytryptamine was greatly reduced in calcium-free buffer, but the breakdown of phosphatidylinositol continued at the same rate in the absence of calcium. These results support the hypothesis that breakdown of phosphatidylinositol by 5-hydroxytryptamine is involved in the gating of calcium.