Stahl R A, Kudelka S
Clin Nephrol. 1986;25 Suppl 1:S78-82.
Immunoreactive prostaglandin E2 (PGE2) formation of rat renal papilla and isolated glomeruli was determined following chronic cyclosporine A treatment (25 and 50 mg/kg BW/daily for up to 6 weeks). Additionally, the in vitro production of PGE2 and the release of C14-labelled arachidonic acid (AA) products were evaluated in the presence of increasing doses of cyclosporine A (CyA). Renal papillary slices and glomeruli were incubated in Krebs-Ringer-Buffer (KRB) at 37 degrees C under air conditions. PGE2 and C14-labelled AA-metabolites were determined in the incubation medium. Chronic in vivo CyA treatment reduced in vitro renal papillary PGE2 formation significantly. Furthermore, the conversion of AA to PGE2 by isolated glomeruli was significantly lower in rats pretreated with CyA over three weeks. In addition, the stimulatory effect of furosemide on PGE2 formation by isolated glomeruli was impaired following an in vivo CyA treatment for three weeks. In vitro incubation of CyA with renal papilla had no effect on in vitro PGE2 formation or the release of C14-labelled AA-metabolites. The data demonstrate that chronic in vivo treatment with CyA can reduce renal PGE2 formation. This effect might influence PG mediated renal functions.
在慢性环孢素A治疗(25和50毫克/千克体重/每日,持续6周)后,测定大鼠肾乳头和分离肾小球的免疫反应性前列腺素E2(PGE2)生成。此外,在递增剂量的环孢素A(CyA)存在的情况下,评估PGE2的体外产生以及C14标记的花生四烯酸(AA)产物的释放。肾乳头切片和肾小球在37℃的空气条件下于 Krebs-Ringer缓冲液(KRB)中孵育。在孵育培养基中测定PGE2和C14标记的AA代谢产物。慢性体内CyA治疗显著降低了体外肾乳头PGE2的生成。此外,在经CyA预处理三周的大鼠中,分离肾小球将AA转化为PGE2的能力显著降低。另外,在体内CyA治疗三周后,速尿对分离肾小球PGE2生成的刺激作用受损。CyA与肾乳头的体外孵育对体外PGE2生成或C14标记的AA代谢产物的释放没有影响。数据表明,慢性体内CyA治疗可降低肾脏PGE2的生成。这种效应可能会影响PG介导的肾脏功能。