Fujimura A, Sudoh T, Ebihara A
Department of Clinical Pharmacology, Jichi Medical School, Tochigi, Japan.
Life Sci. 1994;55(9):707-11. doi: 10.1016/0024-3205(94)00678-4.
The present study was undertaken to examine an effect of an angiotensin II type 1 (AT1) receptor antagonist on urinary prostaglandin E2 (PGE2) excretion following furosemide, a loop diuretic, in rats. Furosemide (30 mg/kg) was given orally with or without pretreatment with derapril (30 mg/kg), an angiotensin converting enzyme inhibitor, TCV-116 (1 mg/kg), an AT1 receptor antagonist, or losartan (10 mg/kg), another AT1 receptor antagonist. The 6-hour urine was collected following furosemide, and the urinary excretion of PGE2 was determined. The urinary PGE2 increased significantly following furosemide alone. However, such a furosemide-induced increase was not observed with pretreatment with derapril, TCV-116 or losartan. These results suggest that the increased urinary excretion of PGE2 following furosemide is blunted by derapril, TCV-116 and losartan. As TCV-116 and losartan are selective AT1 receptor antagonists, the effect of furosemide on renal PGE2 production, as reflected by the urinary PGE2, might be mediated by an activation of AT1 receptors.
本研究旨在检测血管紧张素II 1型(AT1)受体拮抗剂对速尿(一种髓袢利尿剂)给药后大鼠尿中前列腺素E2(PGE2)排泄的影响。速尿(30毫克/千克)经口给药,同时给予或不给予以下预处理:地拉普利(30毫克/千克,一种血管紧张素转换酶抑制剂)、TCV-116(1毫克/千克,一种AT1受体拮抗剂)或氯沙坦(10毫克/千克,另一种AT1受体拮抗剂)。速尿给药后收集6小时尿液,并测定尿中PGE2的排泄量。单独使用速尿后尿中PGE2显著增加。然而,地拉普利、TCV-116或氯沙坦预处理后未观察到速尿引起的这种增加。这些结果表明,地拉普利、TCV-116和氯沙坦可减弱速尿给药后尿中PGE2排泄的增加。由于TCV-116和氯沙坦是选择性AT1受体拮抗剂,速尿对肾PGE2产生的影响(以尿中PGE2反映)可能是由AT1受体的激活介导的。