Michel M C, Feth F, Stieneker M, Rascher W
Department of Medicine, University of Essen, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1992 Apr;345(4):370-4. doi: 10.1007/BF00176612.
We have compared the mechanism of NPY- and carbachol-stimulated Ca2+ increases in SK-N-MC cells. NPY stimulated Ca2+ mobilization via a pertussis toxin-sensitive mechanism. Carbachol stimulated Ca2+ mobilization and influx via pertussis toxin-insensitive and -sensitive mechanisms, respectively. Carbachol but not NPY stimulated inositol phosphate accumulation by a pertussis toxin-insensitive mechanism. We conclude that carbachol promotes Ca2+ influx via a pertussis toxin-sensitive G protein and Ca2+ mobilization via a pertussis toxin-insensitive G-protein coupling to inositol phosphate generation; NPY stimulates Ca2+ mobilization via a pertussis toxin-sensitive G protein without apparent involvement of inositol phosphates.
我们比较了神经肽Y(NPY)和卡巴胆碱刺激SK-N-MC细胞内钙离子增加的机制。NPY通过一种对百日咳毒素敏感的机制刺激钙离子动员。卡巴胆碱分别通过对百日咳毒素不敏感和敏感的机制刺激钙离子动员和内流。卡巴胆碱通过一种对百日咳毒素不敏感的机制刺激肌醇磷酸积累,而NPY则无此作用。我们得出结论,卡巴胆碱通过对百日咳毒素敏感的G蛋白促进钙离子内流,并通过与肌醇磷酸生成偶联的对百日咳毒素不敏感的G蛋白促进钙离子动员;NPY通过对百日咳毒素敏感的G蛋白刺激钙离子动员,而肌醇磷酸显然未参与其中。