Grasa Laura, Arruebo M Pilar, Plaza Miguel A, Murillo M Divina
Department of Pharmacology and Physiology, Faculty of Veterinary Medicine, University of Zaragoza, Miguel Servet 177, 50013 Zaragoza, Spain.
Prostaglandins Other Lipid Mediat. 2006 May;79(3-4):206-17. doi: 10.1016/j.prostaglandins.2006.01.001. Epub 2006 Mar 3.
The effects of PGE(2) on longitudinal smooth muscle, the intracellular mechanisms involved, and the localization of EP receptors were investigated in rabbit small intestine. PGE(2) evoked contractions in small intestine that were reduced by tetrodotoxin and hexamethonium. 17-Phenyl trinor PGE(2), sulprostone, misoprostol and 16,16-dimethyl PGE(2) evoked contractions. Butaprost did not modify spontaneous motility. AH 6809 reduced PGE(2) and 17-phenyl trinor PGE(2)-induced contractions. Verapamil, Ca(2+) free medium, staurosporine, forskolin, theophylline, and rolipram diminished, while IP-20 and H-89 increased PGE(2)-induced contractions. Western blot analysis showed protein bands of 41kDa for EP(1), 71kDa for EP(2) and 62kDa for EP(3) receptors. EP(1), EP(2) and EP(3) receptors were detected in neurons of the myenteric and submucosal ganglia, but only EP(3) receptors were found in smooth muscle layers. This study did not detect EP(4) receptor. PGE(2)-induced contractions would be mediated through EP(1) and EP(3) receptors, and voltage-dependent Ca(2+) channels, protein kinase C, and cAMP would be implicated in these responses.
在兔小肠中研究了前列腺素E2（PGE2）对纵行平滑肌的作用、所涉及的细胞内机制以及EP受体的定位。PGE2引起小肠收缩，这种收缩可被河豚毒素和六甲铵减弱。17-苯基三降PGE2、硫前列酮、米索前列醇和16,16-二甲基PGE2引起收缩。布他前列素不改变自发运动。AH 6809减弱PGE2和17-苯基三降PGE2诱导的收缩。维拉帕米、无钙培养基、星形孢菌素、福斯可林、茶碱和咯利普兰减弱，而IP-20和H-89增强PGE2诱导的收缩。蛋白质印迹分析显示EP1受体的蛋白条带为41kDa，EP2受体为71kDa，EP3受体为62kDa。在肌间神经节和黏膜下神经节的神经元中检测到EP1、EP2和EP3受体，但仅在平滑肌层中发现EP3受体。本研究未检测到EP4受体。PGE2诱导的收缩将通过EP1和EP3受体介导，电压依赖性钙通道、蛋白激酶C和环磷酸腺苷参与这些反应。
