Changya L, Gallacher D V, Irvine R F, Petersen O H
MRC Secretory Control Research Group, University of Liverpool, England.
FEBS Lett. 1989 Jul 17;251(1-2):43-8. doi: 10.1016/0014-5793(89)81425-5.
In internally perfused single lacrimal acinar cells the competitive inositol 1,4,5-trisphosphate (Ins 1,4,5-P3)-antagonist heparin inhibits the ACh-evoked K+ current response mediated by internal Ca2+ and also blocks both the Ins 1,4,5-P3-evoked transient as well as the sustained K+ current increase evoked by combined stimulation with internal Ins 1,4,5-P3 and inositol 1,3,4,5-tetrakisphosphate (Ins 1,3,4,5-P4). When, during sustained stimulation with both Ins 1,4,5-P3 and Ins 1,3,4,5-P4, one of the inositol polyphosphates is removed, the K+ current declines; whereas removal of Ins 1,4,5-P3 results in an immediate termination of the response, removal of Ins 1,3,4,5-P4 only causes a very gradual and slow reduction in the current. Ins 1,3,4,5-P4 is therefore not an acute controller of Ca2+ release from stores into the cytosol, but modulates the release of Ca2+ induced by Ins 1,4,5,P3 by an unknown mechanism, perhaps by linking Ins 1,4,5 P3-sensitive and insensitive Ca2+ stores.
在内部灌注的单个泪腺腺泡细胞中，竞争性肌醇1,4,5 -三磷酸（Ins 1,4,5 - P3）拮抗剂肝素可抑制由细胞内Ca2+介导的乙酰胆碱（ACh）诱发的钾离子电流反应，并且还能阻断Ins 1,4,5 - P3诱发的瞬态反应以及由细胞内Ins 1,4,5 - P3和肌醇1,3,4,5 -四磷酸（Ins 1,3,4,5 - P4）联合刺激诱发的持续性钾离子电流增加。当在Ins 1,4,5 - P3和Ins 1,3,4,5 - P4持续刺激过程中去除其中一种肌醇多磷酸时，钾离子电流会下降；去除Ins 1,4,5 - P3会导致反应立即终止，而去除Ins 1,3,4,5 - P4只会使电流非常缓慢且逐渐地降低。因此，Ins 1,3,4,5 - P4不是从储存库向细胞质中释放Ca2+的急性调控因子，而是通过一种未知机制调节由Ins 1,4,5 - P3诱导的Ca2+释放，可能是通过连接Ins 1,4,5 - P3敏感和不敏感的Ca2+储存库来实现的。
