Fujimoto N, Shichi H
Kresge Eye Institute, Department of Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan, USA.
J Ocul Pharmacol Ther. 1996 Fall;12(3):343-51. doi: 10.1089/jop.1996.12.343.
Porcine iris sphincter muscle strips contracted in response to carbachol. The tissue contraction was inhibited by prostaglandin (PG) E2 but not by PGF2 alpha. In order to investigate the effect of PGs on the iris cells, the porcine sphincter muscle cells were grown in culture to a confluence and characterized. Using the secondary culture of cells, the effect of PGs on carbachol-induced cell contraction was investigated. Both PGE2 and PGF2 alpha at 100 microM blocked cell contraction completely. The concentration required to inhibit 50% of the maximum contraction in 15 minutes was 10(-6) M for PGE2 and 10(-6)-10(-7) M for PGF2 alpha. Using PGE2 receptor subtype agonists (EP2 agonist, 11-deoxy-16, 16 dimethyl PGE2 and EP3 agonist, sulprostone), PGE2 receptor involved in the inhibition of carbachol-induced contraction was identified to be of the EP2 subtype. In support of this characterization, the addition of PGE2 to cultured porcine sphincter muscle cells increased intracellular cAMP level. The discrepancy in PGF2 alpha effect on carbachol-induced sphincter muscle contraction between iris tissue strips and cultured cells suggests that nonmuscular cells may be involved in the modulation of the PGF2 alpha effect on sphincter muscle cells in vivo.
猪虹膜括约肌条对卡巴胆碱产生收缩反应。组织收缩受到前列腺素（PG）E2的抑制，但不受PGF2α的抑制。为了研究PGs对虹膜细胞的影响，将猪括约肌细胞在培养物中培养至汇合状态并进行表征。利用细胞的传代培养，研究了PGs对卡巴胆碱诱导的细胞收缩的影响。100微摩尔的PGE2和PGF2α均可完全阻断细胞收缩。15分钟内抑制最大收缩50%所需的浓度，PGE2为10^(-6) M，PGF2α为10^(-6)-10^(-7) M。使用PGE2受体亚型激动剂（EP2激动剂，11-脱氧-16,16-二甲基PGE2和EP3激动剂，舒前列素），确定参与抑制卡巴胆碱诱导收缩的PGE2受体为EP2亚型。作为这一特性的佐证，向培养的猪括约肌细胞中添加PGE2可提高细胞内cAMP水平。虹膜组织条和培养细胞中PGF2α对卡巴胆碱诱导的括约肌收缩作用的差异表明，非肌肉细胞可能参与了体内PGF2α对括约肌细胞作用的调节。
