Kopp U C, Farley D M, Smith L A, Knapp H R
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City.
Am J Physiol. 1995 Jan;268(1 Pt 2):R164-70. doi: 10.1152/ajpregu.1995.268.1.R164.
The role of prostaglandins in renal sensory receptor activation was examined in rats fed an essential fatty acid-deficient (EFAD) diet to cause tissue arachidonate depletion. Littermates fed a standard diet were used as controls. In anesthetized rats, the increases in afferent renal nerve activity due to increasing ureteral pressure 2.5, 5, 7.5, 10, 12.5, and 15 mmHg were significantly reduced by the EFAD diet (P < 0.02): 3 +/- 5, 3 +/- 5, 11 +/- 5, 9 +/- 5, 19 +/- 3, and 17 +/- 5%, respectively, in EFAD rats and 23 +/- 11, 36 +/- 15, 50 +/- 15, 52 +/- 8, 72 +/- 17, and 90 +/- 19%, respectively, in control rats. In EFAD rats, addition of prostaglandin E2 (PGE2) to the renal pelvic perfusate restored the afferent renal nerve activity response to increased ureteral pressure toward that in control rats. PGE2 had no effect in control rats. Also the afferent renal nerve activity responses to renal pelvic perfusion with bradykinin at 4, 20, 100, and 500 micrograms/ml were significantly suppressed by the EFAD diet (P < 0.01): 13 +/- 15, 5 +/- 7, 60 +/- 19, and 63 +/- 20%, respectively, in EFAD rats and 122 +/- 23, 142 +/- 31, 172 +/- 19, and 190 +/- 39%, respectively, in control rats. These results demonstrate an important role for arachidonate metabolites, particularly PGE2, in renal sensory receptor activation. Together with our previous studies showing that indomethacin blocks the afferent renal nerve activity responses to increased ureteral pressure or bradykinin, the present studies provide strong evidence for an essential role of prostaglandins in renal sensory receptor activation.
通过给大鼠喂食缺乏必需脂肪酸（EFAD）的饮食以导致组织花生四烯酸耗竭，研究了前列腺素在肾感觉受体激活中的作用。喂食标准饮食的同窝大鼠用作对照。在麻醉的大鼠中，EFAD饮食显著降低了因输尿管压力分别增加2.5、5、7.5、10、12.5和15 mmHg而引起的肾传入神经活动增加（P<0.02）：EFAD大鼠分别为3±5、3±5、11±5、9±5、19±3和17±5%，对照大鼠分别为23±11、36±15、50±15、52±8、72±17和90±19%。在EFAD大鼠中，向肾盂灌注液中添加前列腺素E2（PGE2）可使肾传入神经活动对输尿管压力增加的反应恢复至对照大鼠的水平。PGE2对对照大鼠无影响。此外，EFAD饮食显著抑制了肾传入神经活动对肾盂灌注4、20、100和500微克/毫升缓激肽的反应（P<0.01）：EFAD大鼠分别为13±15、5±7、60±19和63±20%，对照大鼠分别为122±23、142±31、172±19和190±39%。这些结果表明花生四烯酸代谢产物，特别是PGE2，在肾感觉受体激活中起重要作用。与我们之前的研究表明吲哚美辛可阻断肾传入神经活动对输尿管压力增加或缓激肽的反应一起，本研究为前列腺素在肾感觉受体激活中的重要作用提供了有力证据。
