Spokas E G, Wong P Y, McGiff J C
Hypertension. 1982 May-Jun;4(3 Pt 2):96-100.
The possibility that 6-keto-prostaglandin E1 (6-keto-PGE1) affects renin release was studied using rabbit renal cortical slices, a preparation that eliminates hemodynamic, neural, and blood-borne factors that might influence renin release. The medium used for incubating the slices was collected for renin assay at the end of each of four successive 20-minute periods. Test agents were added only once, at the beginning of Period 3 (experimental period). Between Periods 3 an 4 (recovery period), the medium was aspirated and the slices rinsed with Krebs solution before replacing the medium. Renin release did not change in vehicle-treated slices. Unlike the PGI2-induced changes, the effects of 6-keto-PGE1 on renin release were sustained in Period 4. Indomethacin potentiated renin stimulation induced by 10 microM concentrations of PGI2 and 6-keto-PGE1 in Period 3 and by 6-keto-PGE1 in Period 4. Using platelet antiaggregatory activity as an index of stability, we found that PGI2 was largely inactivated within 10 minutes under the conditions used for incubating the slices (pH 7.4, 37 degrees C), while 6-keto-PGE1 was stable. The results lend further support to the concept that 6-keto PgE1 is capable of releasing renin through a direct action.
利用兔肾皮质切片研究了6-酮-前列腺素E1(6-keto-PGE1)影响肾素释放的可能性,该制备方法消除了可能影响肾素释放的血流动力学、神经和血源性因素。在连续四个20分钟时间段结束时,收集用于孵育切片的培养基进行肾素测定。测试剂仅在第3阶段(实验期)开始时添加一次。在第3阶段和第4阶段(恢复期)之间,吸出培养基,并用Krebs溶液冲洗切片,然后更换培养基。在载体处理的切片中,肾素释放没有变化。与PGI2诱导的变化不同,6-keto-PGE1对肾素释放的影响在第4阶段持续存在。吲哚美辛增强了第3阶段10 microM浓度的PGI2和6-keto-PGE1以及第4阶段6-keto-PGE1诱导的肾素刺激。以血小板抗聚集活性作为稳定性指标,我们发现在用于孵育切片的条件下(pH 7.4,37℃),PGI2在10分钟内大部分失活,而6-keto-PGE1是稳定的。这些结果进一步支持了6-酮-PgE1能够通过直接作用释放肾素的概念。