Fukuda T, Arakawa T, Mach T, Durbin T, Tarnawski A
Gastroenterology Section, Veterans Administration Medical Center, Long Beach, California 90822.
Prostaglandins. 1991 Dec;42(6):587-97. doi: 10.1016/0090-6980(91)90020-g.
We investigated the effects of calcium channel blockers on generation of prostaglandin (PG) E2 and 6-keto PGF1 alpha by gastric mucosal surface epithelium. Surface epithelial cells (SEC) isolated from rat gastric mucosa were incubated with either verapamil (1 or 10 micrograms/ml), diltiazem (2.5 or 25 micrograms/ml) or nifedipine (2.5 or 25 micrograms/ml) for 30 min at 37 degrees C in calcium containing or calcium-free medium. Verapamil (both doses) significantly increased PGE2 and 6-keto PGF1 alpha generation by the surface epithelial cells but only in calcium containing medium. Diltiazem did not affect PG generation in calcium containing nor calcium-free medium. Nifedipine 25 micrograms/ml decreased PGE2 but increased 6-keto PGF1 alpha generation. The inhibitory effect of nifedipine on PGE2 generation was abolished in calcium-free medium, while the calmodulin antagonist did not affect verapamil-induced increase in PG generation.
我们研究了钙通道阻滞剂对胃黏膜表面上皮细胞生成前列腺素(PG)E2和6-酮-前列腺素F1α的影响。从大鼠胃黏膜分离的表面上皮细胞(SEC),在含或不含钙的培养基中,于37℃分别与维拉帕米(1或10微克/毫升)、地尔硫䓬(2.5或25微克/毫升)或硝苯地平(2.5或25微克/毫升)孵育30分钟。维拉帕米(两种剂量)均显著增加表面上皮细胞生成PGE2和6-酮-前列腺素F1α,但仅在含钙培养基中。地尔硫䓬在含或不含钙的培养基中均不影响PG生成。25微克/毫升硝苯地平降低PGE2生成,但增加6-酮-前列腺素F1α生成。硝苯地平对PGE2生成的抑制作用在无钙培养基中消失,而钙调蛋白拮抗剂不影响维拉帕米诱导的PG生成增加。