Fowler C J, Brännström G
Department of Biochemical Pharmacology, Astra Pain Control AB, Preclinical R&D, Huddinge, Sweden.
Methods Find Exp Clin Pharmacol. 1994 Jan-Feb;16(1):21-8.
The effects of substance P (SP) upon basal and forskolin-stimulated cAMP production have been investigated in UC11MG cells. The cells expressed 40,000 NK1 receptors/cell, the stimulation of which led to enhanced phosphoinositide breakdown. Forskolin (10 and 100 mcM) stimulated cAMP production, whereas SP (3 and 300 nM) produced no significant increase in cAMP production. However, SP enhanced the response to forskolin, with an EC50 value of about 10 nM. The response to forskolin was also enhanced by physalaemin and eledoisin, and was sensitive to inhibition by (+/-)CP96345. It is concluded that in the UC11MG cell line, SP not only stimulates phosphoinositide breakdown but also enhances the cAMP response to forskolin, possibly via stimulation of NK1 receptors.
已在UC11MG细胞中研究了P物质（SP）对基础和福斯高林刺激的环磷酸腺苷（cAMP）生成的影响。这些细胞每个细胞表达40,000个神经激肽1（NK1）受体，对其刺激会导致磷酸肌醇分解增强。福斯高林（10和100微摩尔）刺激cAMP生成，而SP（3和300纳摩尔）未使cAMP生成显著增加。然而，SP增强了对福斯高林的反应，半数有效浓度（EC50）值约为10纳摩尔。雨蛙肽和蛙皮素也增强了对福斯高林的反应，且该反应对（±）CP96345的抑制敏感。得出的结论是，在UC11MG细胞系中，SP不仅刺激磷酸肌醇分解，还可能通过刺激NK1受体增强对福斯高林的cAMP反应。
