Tepperman B L, Tepperman F S, Fang W F, Jacobson E D
Can J Physiol Pharmacol. 1978 Oct;56(5):834-9. doi: 10.1139/y78-131.
The actions of 16,16-dimethyl prostaglandin E2 (dmPGE2) were investigated on ion transport in in vitro rabbit fundic mucosa and rat isolated jejunal cells. Addition of dmPGE2 (1.3 X 10(-4)M) to the serosal side of the rabbit mucosa resulted in a significant decrease in the transmural potential difference (PD) and short circuit current (Isc). The transmembrane resistance (R) displayed a significant rise over control values. Furthermore, the net serosa to mucosa flux of chloride ion decreased while the net serosa to mucosa movement of sodium remained unchanged. In the rat intestinal cells, increasing the concentration of dmPGE2 from 10(-10) to 10(-4)M caused a fall in sodium efflux. These data indicate that dmPGE2 alters the rate of active transport of the predominant ion pump of the resting rabbit gastric mucosa and the rate of Na efflux from rat intestinal epithelial cells without apparently affecting the membrane permeability.
研究了16,16 - 二甲基前列腺素E2(dmPGE2)对体外兔胃底黏膜和大鼠离体空肠细胞离子转运的作用。将dmPGE2(1.3×10⁻⁴M)添加到兔黏膜浆膜侧,导致跨壁电位差(PD)和短路电流(Isc)显著降低。跨膜电阻(R)相较于对照值显著升高。此外,氯离子从浆膜到黏膜的净通量降低,而钠离子从浆膜到黏膜的净移动保持不变。在大鼠肠道细胞中,将dmPGE2浓度从10⁻¹⁰提高到10⁻⁴M会导致钠外流减少。这些数据表明,dmPGE2改变了静息兔胃黏膜主要离子泵的主动转运速率以及大鼠肠道上皮细胞的钠外流速率,而对膜通透性无明显影响。