Kopp U C, Farley D M, Smith L A
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, USA.
Am J Physiol. 1996 Apr;270(4 Pt 2):R720-7. doi: 10.1152/ajpregu.1996.270.4.R720.
Renal mechanoreceptor (MR) activation by increased ureteral pressure (increases UP) results in an increase in afferent renal nerve activity (ARNA) that is blocked by substance P receptor blockade and prostaglandin (PG) synthesis inhibition. To examine the interaction between substance P and PGs, the release of substance P and PGE into the renal pelvis was studied before and during renal pelvic perfusion with indomethacin. Before indomethacin, increases UP increased ARNA 43 +/- 6% and renal pelvic release of substance P from 11 +/- 3 to 29 +/- 8 pg/min and PGE from 319 +/- 71 to 880 +/- 146 pg/min. Indomethacin blocked the increases in ARNA and release of substance P and PGE produced by increases UP. Time control experiments showed reproducible increases in ARNA and release of substance P and PGE during increases UP. Mechanical stimulation of the renal pelvic wall in vitro resulted in an increase in PGE release from 110 +/- 8 to 722 +/- 152 pg/min, which was abolished by indomethacin, suggesting a de novo PGE synthesis. The data suggest that increases UP results in a renal pelvic release of PGE, which facilitates the release of substance P and activation of renal pelvic MR.
输尿管压力升高（增加UP）激活肾机械感受器（MR）会导致肾传入神经活动（ARNA）增加，而这种增加会被P物质受体阻断和前列腺素（PG）合成抑制所阻断。为了研究P物质与PG之间的相互作用，在肾盂灌注消炎痛之前和期间，研究了肾盂中P物质和PGE的释放情况。在使用消炎痛之前，UP增加使ARNA增加43±6%，肾盂中P物质的释放从11±3 pg/min增加到29±8 pg/min，PGE从319±71 pg/min增加到880±146 pg/min。消炎痛阻断了UP增加所导致的ARNA增加以及P物质和PGE的释放。时间对照实验表明，在UP增加期间，ARNA以及P物质和PGE的释放会出现可重复的增加。体外对肾盂壁的机械刺激使PGE释放从110±8 pg/min增加到722±152 pg/min，这一增加被消炎痛消除，提示有新的PGE合成。数据表明，UP增加导致肾盂释放PGE，这促进了P物质的释放以及肾盂MR的激活。
