Blasingham M C, Shade R E, Share L, Nasjletti A
J Pharmacol Exp Ther. 1980 Jul;214(1):1-4.
We compared the effects of sodium meclofenamate (5 mg/kg i.v.), an inhibitor of prostaglandin synthesis, on renal function in six unanesthetized dogs maintained for 5 to 7 days before the experiment on 100 mEq/day of NaCl and after sodium depletion by furosemide administration and salt deprivation. Plasma renin activity (PRA) during sodium depletion (12.35 +/- 3.93 ng ml-1 hr-1) was higher than during sodium repletion (1.46 +/- 0.47 ng ml-1 hr-1; P less than .05). The administration of meclofenamate did not alter mean arterial pressure, renal blood flow, urine volume, excretion of sodium and potassium or PRA in the sodium replete dog. However, during sodium depletion meclofenamate reduced renal blood flow from 168 +/- 35 to 105 +/- 23 ml/min (P less than .01) and urine flow from 0.32 +/- 0.09 to 0.16 +/- 0.05 ml/min (P less than .05) but did not affect mean arterial pressure, electrolyte excretion or PRA. The meclofenamate-induced reduction in renal blood flow during sodium depletion was well correlated with control PRA. After administration of meclofenamate, the urinary excretion of immunoreactive prostaglandin E2 fell by 66% (P less than .05) in the sodium replete dog and by 72% (P less than .05) in the sodium depleted dog. This study demonstrates that the effects of meclofenamate on renal hemodynamics vary with the state of sodium balance and in relation to PRA.
我们比较了氯灭酸（5毫克/千克静脉注射）（一种前列腺素合成抑制剂）对6只未麻醉犬肾功能的影响。这些犬在实验前5至7天每天维持摄入100毫当量氯化钠，之后通过给予速尿和限制盐摄入使钠缺失。钠缺失期间的血浆肾素活性（PRA）（12.35±3.93纳克/毫升·小时）高于钠补充期间（1.46±0.47纳克/毫升·小时；P＜0.05）。在钠补充的犬中，给予氯灭酸未改变平均动脉压、肾血流量、尿量、钠和钾的排泄或PRA。然而，在钠缺失期间，氯灭酸使肾血流量从168±35降至105±23毫升/分钟（P＜0.01），尿流量从0.32±0.09降至0.16±0.05毫升/分钟（P＜0.05），但不影响平均动脉压、电解质排泄或PRA。氯灭酸在钠缺失期间引起的肾血流量减少与对照PRA密切相关。给予氯灭酸后，钠补充犬的免疫反应性前列腺素E2尿排泄量下降66%（P＜0.05），钠缺失犬下降72%（P＜0.05）。本研究表明，氯灭酸对肾血流动力学的影响随钠平衡状态以及与PRA相关而变化。
