Marc S, Leiber D, Harbon S
FEBS Lett. 1986 May 26;201(1):9-14. doi: 10.1016/0014-5793(86)80561-0.
In the guinea pig myometrium prelabelled with myo-[2-3H]inositol, carbachol and oxytocin enhanced a concentration-dependent and rapid release of IP3 which preceded that of IP2 and IP1. The specific receptor-mediated phospholipase C activation degrading PIP2 to IP3 did not require the presence of extracellular Ca2+. The ionophore A23187 as well as K+ depolarization failed to increase inositol phosphate accumulation. It is proposed that IP3 could have a role in the contraction of uterine smooth muscle elicited by the activation of muscarinic as well as of oxytocin receptors.
在预先用肌醇-[2-³H]标记的豚鼠子宫肌层中,卡巴胆碱和催产素可增强肌醇三磷酸(IP3)浓度依赖性的快速释放,且这种释放先于肌醇二磷酸(IP2)和肌醇一磷酸(IP1)。特异性受体介导的磷脂酶C激活将磷脂酰肌醇-4,5-二磷酸(PIP2)降解为IP3并不需要细胞外钙离子的存在。离子载体A23187以及钾离子去极化均未能增加肌醇磷酸的积累。有人提出,IP3可能在毒蕈碱受体和催产素受体激活所引发的子宫平滑肌收缩中发挥作用。