Baird J G, Chilvers E R, Kennedy E D, Nahorski S R
Department of Pharmacology, University of Leicester, United Kingdom.
Naunyn Schmiedebergs Arch Pharmacol. 1989 Mar;339(3):247-51. doi: 10.1007/BF00173572.
The effect of changes in extracellular calcium concentration ([Ca2+]e) on the incorporation of myo-[2-3H]-inositol into phosphoinositides and agonist-stimulated 3H-inositol phosphates (3H-InsPs) was examined in rat cerebral cortex and bovine tracheal smooth muscle slices. In brain slices, reduction in [Ca2+]e from 2.4 to 1.2 mmol/l resulted in an approximate doubling of the carbachol and noradrenaline-stimulated 3H-InsP response with no effect on the EC50 values. An identical effect of varying [Ca2+]e was observed for carbachol-stimulated 3H-InsP formation in tracheal smooth muscle with a further increase in 3H-InsPs evident at [Ca2+]e 0.6 mmol/l. In this tissue the effect of changes in [Ca2+]e on the incorporation of myo-[2-3H]-inositol into the total phosphoinositide pool directly paralleled the changes in 3H-InsPs except in conditions of no added calcium when 3H-InsP responses were markedly impaired. Additional studies in brain slices using buffer where the added calcium varied between 0 and 2.4 mmol/l, showed that both the carbachol stimulated formation of separate inositol phosphates during short incubation periods and incorporation of myo-[2-3H]-inositol into PtdInsP and PtdInsP2 under basal conditions was maximal at [Ca2+]e 0.3 mmol/l. Omitting Ca2+ from the buffer resulted in maximal labelling of PtdIns but a decrease in PtdInsP and PtdInsP2 labelling (compared with the level at [Ca2+]e 0.3 mmol/l) and a markedly impaired inositol polyphosphate response. Alterations in [Ca2+]e following 3H-inositol labelling but immediately prior to carbachol stimulation did not influence 3H-inositol polyphosphate responses. It is therefore clear that even relatively small changes in [Ca2+]e markedly influence agonist-stimulated 3H-InsP responses in brain and tracheal smooth muscle slices and that these reflect changes in the labelling of substrate inositol lipids.(ABSTRACT TRUNCATED AT 250 WORDS)
在大鼠大脑皮层和牛气管平滑肌切片中,研究了细胞外钙浓度([Ca2+]e)变化对肌醇-[2-3H]-肌醇掺入磷酸肌醇以及激动剂刺激的3H-肌醇磷酸(3H-InsPs)的影响。在脑切片中,[Ca2+]e从2.4 mmol/l降至1.2 mmol/l,导致卡巴胆碱和去甲肾上腺素刺激的3H-InsP反应增加约一倍,而对EC50值无影响。在气管平滑肌中,观察到[Ca2+]e变化对卡巴胆碱刺激的3H-InsP形成有相同作用,在[Ca2+]e为0.6 mmol/l时3H-InsPs进一步增加。在该组织中,[Ca2+]e变化对肌醇-[2-3H]-肌醇掺入总磷酸肌醇池的影响与3H-InsPs的变化直接平行,除了在不添加钙的情况下,3H-InsP反应明显受损。在脑切片中使用添加钙在0至2.4 mmol/l之间变化的缓冲液进行的额外研究表明,在短孵育期内卡巴胆碱刺激形成单独的肌醇磷酸以及在基础条件下肌醇-[2-3H]-肌醇掺入磷脂酰肌醇磷酸(PtdInsP)和磷脂酰肌醇二磷酸(PtdInsP2)在[Ca2+]e为0.3 mmol/l时最大。从缓冲液中省略Ca2+导致磷脂酰肌醇(PtdIns)标记最大,但PtdInsP和PtdInsP2标记减少(与[Ca2+]e为0.3 mmol/l时的水平相比),并且肌醇多磷酸反应明显受损。在3H-肌醇标记后但在卡巴胆碱刺激之前[Ca2+]e的改变不影响3H-肌醇多磷酸反应。因此,很明显,即使[Ca2+]e相对较小的变化也会显著影响脑和气管平滑肌切片中激动剂刺激的3H-InsP反应,并且这些反应反映了底物肌醇脂质标记的变化。(摘要截断于250字)