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. 1997 Jun;272(6 Pt 2):R2009-16. doi: 10.1152/ajpregu.1997.272.6.R2009.
In anesthetized rats, renal pelvic administration of bradykinin results in a prostaglandin (PG)-dependent increase in afferent renal nerve activity (ARNA). We now measured renal pelvic release of PGE and substance P during renal pelvic administration of bradykinin. Bradykinin increased ARNA and renal pelvic release of PGE by 497 +/- 252 pg/min and substance P. by 10.7 +/- 7.2 pg/min. Renal pelvic perfusion with indomethacin abolished the bradykinin-mediated increase in ARNA and reduced renal pelvic release of PGE and substance P by 76 +/- 11 and 72 +/- 8%, respectively. To examine whether the increased substance P release contributed to bradykinin-mediated activation of renal sensory receptors, renal pelvis was perfused with the substance P-receptor antagonists CP-96,345, CP-99,994, or RP-67580. The ARNA response to bradykinin was reduced 73 +/- 11, 55 +/- 12, and 64 +/- 10% by CP-96,345, CP-99,994, and RP-67580, respectively. The inactive enantiomers CP-96,344 and RP-68651 had no effect. These data suggest that bradykinin increases renal pelvic release of PGE, which facilitates the release of substance P, which in turn stimulates substance P receptors. Thus the ARNA response to bradykinin is largely mediated by activation of substance P receptors.
在麻醉大鼠中，向肾盂内注射缓激肽会导致肾传入神经活动（ARNA）依赖前列腺素（PG）而增加。我们现在测量了在向肾盂内注射缓激肽期间肾盂中前列腺素E（PGE）和P物质的释放情况。缓激肽使ARNA增加，肾盂中PGE的释放量增加了497±252 pg/分钟，P物质的释放量增加了10.7±7.2 pg/分钟。用吲哚美辛灌注肾盂消除了缓激肽介导的ARNA增加，并使肾盂中PGE和P物质的释放量分别减少了76±11%和72±8%。为了研究P物质释放增加是否有助于缓激肽介导的肾感觉受体激活，用P物质受体拮抗剂CP-96,345、CP-99,994或RP-67580灌注肾盂。CP-96,345、CP-99,994和RP-67580分别使对缓激肽的ARNA反应降低了73±11%、55±12%和64±10%。无活性对映体CP-96,344和RP-68651没有作用。这些数据表明，缓激肽增加了肾盂中PGE的释放，这促进了P物质的释放，而P物质又刺激P物质受体。因此，对缓激肽的ARNA反应很大程度上是由P物质受体的激活介导的。
