Abe Y, Okahara T, Miura K, Yukimura T, Takada T, Iwatani T, Iso T, Yamamoto K
Naunyn Schmiedebergs Arch Pharmacol. 1984 Apr;325(4):356-9. doi: 10.1007/BF00504381.
The renal excretory mechanism of an orally active inhibitor of angiotensin converting enzyme (SA-446) was examined in anesthetized dogs. Parenteral administration of this compound resulted in production of constant levels of about 2 mg/l in the plasma (PSA) and the urine concentration was 726 +/- 200 mg/l, a level significantly higher than that in the plasma. Renal clearance of SA-446 (CSA) was 2.24 +/- 0.34 ml/g X min and was significantly higher than GFR. The clearance ratio (CSA/GFR) of over 1.0 was indicative of a net tubular secretion. Administration of probenecid resulted in a significant rise in PSA and in a significant decrease in urinary excretion but with no change in the plasma protein binding ratio. CSA decreased significantly from 2.24 +/- 0.34 to 0.71 +/- 0.14 ml/g X min. The inhibitory action of SA-446 (0.02 mg/kg, i.v.) on the pressor response to angiotensin I disappeared at about 50 min, this action being maintained for about 2 h in the probenecid pretreated dog. Since probenecid is a competitive inhibitor of organic anion secretory transport, our results show the net tubular secretion of SA-446, via organic anion transport systems. Prolongation of the action of SA-446, as induced by probenecid may be due to the increase of plasma concentration, by the inhibition of tubular secretion.
在麻醉犬身上研究了口服活性血管紧张素转换酶抑制剂(SA - 446)的肾脏排泄机制。静脉注射该化合物后,血浆中该化合物水平维持在约2mg/l恒定,尿浓度为726±200mg/l,显著高于血浆浓度。SA - 446的肾清除率(CSA)为2.24±0.34ml/g×min,显著高于肾小球滤过率(GFR)。清除率比值(CSA/GFR)大于1.0表明存在肾小管净分泌。给予丙磺舒后,血浆中SA - 446水平显著升高,尿排泄显著减少,但血浆蛋白结合率无变化。CSA从2.24±0.34显著降至0.71±0.14ml/g×min。静脉注射SA - 446(0.02mg/kg)对血管紧张素I升压反应的抑制作用在约50分钟时消失,而在丙磺舒预处理的犬中,该作用维持约2小时。由于丙磺舒是有机阴离子分泌转运的竞争性抑制剂,我们的结果表明SA - 446通过有机阴离子转运系统进行肾小管净分泌。丙磺舒诱导的SA - 446作用延长可能是由于肾小管分泌受抑制导致血浆浓度升高所致。