Blasingham M C, Nasjletti A
Am J Physiol. 1980 Oct;239(4):F360-F365. doi: 10.1152/ajprenal.1980.239.4.F360.
We studied the renal effects of the cyclooxygenase inhibitor sodium meclofenamate (M) (5 mg/kg, iv) in the pentobarbital-anesthetized dog that had been maintained on an elevated (100 meq/day) or on a reduced (< meq/day) sodium intake, and during the administration of antiotensin II in the sodium-replete dog, or the angiotensin receptor blocker [Sar1-Ala8]angiotensin II in the sodium-deprived dog. In the sodium-replete dog, M did not affect mean arterial blood pressure (MABP), renal blood flow (RBF), glomerular filtration rate, (GFR), or urine volume (V), but reduced the urinary excretion of sodium (UNaV) by 47%, and of immunoreactive PGE2 (iPGE2) by 90%. However, in the sodium-replete dog during angiotensin II infusion (3 ng . kg-1 . min-1, iv), M reduced RBF by 35%, GFR by 24%, V by 72%, and iPGE2 by 94%. Similarly, in the sodium-deprived dog M reduced RBF by 34%, GFR by 28%, and iPGE2 excretion by 89%. However, M did not affect RBF or GFR in the sodium-deprived dog during infusion of [Sar1-Ala8]angiotensin II (6 microgram . kg-1 . min-1, iv), although iPGE2 excretion was reduced by 84%. This study demonstrates that the effects of M on renal hemodynamics in the dog vary with the state of sodium balance and suggests that a prostaglandin(s) contributes to maintenance of renal blood flow during activation of the renin-angiotensin system.
我们研究了环氧化酶抑制剂甲氯芬那酸钠（M）（5毫克/千克，静脉注射）对戊巴比妥麻醉犬的肾脏影响。这些犬分别维持高钠摄入（100毫当量/天）或低钠摄入（<毫当量/天），并且在钠充足的犬给予血管紧张素II期间，或在钠缺乏的犬给予血管紧张素受体阻滞剂[Sar1-Ala8]血管紧张素II期间进行研究。在钠充足的犬中，M不影响平均动脉血压（MABP）、肾血流量（RBF）、肾小球滤过率（GFR）或尿量（V），但钠尿排泄量（UNaV）降低了47%，免疫反应性前列腺素E2（iPGE2）降低了90%。然而，在钠充足的犬静脉输注血管紧张素II（3纳克·千克-1·分钟-1）期间，M使RBF降低了35%，GFR降低了24%，V降低了72%，iPGE2降低了94%。同样，在钠缺乏的犬中，M使RBF降低了34%，GFR降低了28%，iPGE2排泄降低了89%。然而，在钠缺乏的犬静脉输注[Sar1-Ala8]血管紧张素II（6微克·千克-1·分钟-1）期间，M不影响RBF或GFR，尽管iPGE2排泄降低了84%。本研究表明，M对犬肾血流动力学的影响随钠平衡状态而异，并提示一种或多种前列腺素在肾素-血管紧张素系统激活期间有助于维持肾血流量。
