Mizumura Y, Matsumoto M, Nishino A, Takata M, Iida H, Sugimoto T
Ren Physiol. 1984;7(5):299-303. doi: 10.1159/000172949.
The effect of captopril (SQ 14,225) on the renal hemodynamics, cortical plasma flow (CPF) and noncortical plasma flow (NCPF), was studied in sodium-replete anesthetized dogs during aprotinin infusion. Mean blood pressure (MBP) increased by aprotinin (p less than 0.05) and decreased by captopril (p less than 0.02). Renal vascular resistance (RVR) tended to increase by aprotinin and decreased from 1.29 to 0.86 mm Hg/ml/h (74.7%) by captopril (p less than 0.05). Renal vein renin activity (RRA) inclined to decrease by aprotinin and increased from 17.8 to 47.2 ng/ml/h (278.2%) by captopril (p less than 0.05). Although the administration of captopril alone did not alter the renal hemodynamics despite the reduction of MBP, captopril made a recovery of renal plasma flow (RPF), CPF and NCPF which had decreased by aprotinin. Especially, CPF showed a significant recovery from 45.4 to 55.6 ml/min (123.6%) by captopril (p less than 0.02). These results indicate that the inhibition of endogenous angiotensin made a preferential increase in CPF and suggest that the renin-angiotensin system plays a major role in the effect of captopril of the renal hemodynamic changes.
在输注抑肽酶期间，对钠负荷充足的麻醉犬研究了卡托普利（SQ 14,225）对肾血流动力学、皮质血浆流量（CPF）和非皮质血浆流量（NCPF）的影响。抑肽酶使平均血压（MBP）升高（p<0.05），卡托普利使其降低（p<0.02）。抑肽酶使肾血管阻力（RVR）有升高趋势，卡托普利使其从1.29 mmHg/ml/h降至0.86 mmHg/ml/h（74.7%）（p<0.05）。抑肽酶使肾静脉肾素活性（RRA）有降低趋势，卡托普利使其从17.8 ng/ml/h升至47.2 ng/ml/h（278.2%）（p<0.05）。尽管单独给予卡托普利在降低MBP的情况下未改变肾血流动力学，但卡托普利使因抑肽酶而降低的肾血浆流量（RPF）、CPF和NCPF得到恢复。尤其是，卡托普利使CPF从45.4 ml/min显著恢复至55.6 ml/min（123.6%）（p<0.02）。这些结果表明，内源性血管紧张素的抑制使CPF优先增加，并提示肾素-血管紧张素系统在卡托普利对肾血流动力学变化的作用中起主要作用。
