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Articles in PresS, published online ahead of print February 28, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00701.2001
Submitted on November 26, 2001
Accepted on January 31, 2002
* To whom correspondence should be addressed. E-mail: ukopp{at}blue.weeg.uiowa.edu.
Increasing renal pelvic pressure increases afferent renal nerve activity (ARNA) by a prostaglandin E2 (PGE2)-mediated release of substance P (SP) from renal pelvic nerves. The role of cAMP activation in the PGE2-mediated release of SP was studied by examining the effects of the adenylyl cyclase (AC) activator forskolin and AC inhibitor dideoxyadenosine (DDA). Forskolin enhanced the bradykinin-mediated release of SP from an isolated rat renal pelvic wall preparation, from 7.3±1.3 to 15.6±3.0 pg/min. PGE2 at a subtreshold concentration for SP release mimicked the effects of forskolin. The EP2 receptor agonist butaprost, 15 µM, and PGE2, 0.14 µM, produced similar increases in SP release, from 5.8±0.8 to 17.0±2.3 pg/min and from 8.0±1.3 to 21.6±2.7 pg/min. DDA blocked the SP release produced by butaprost and PGE2. The PGE2-induced release of SP was also blocked by the PKA inhibitors PKI14-22 and H-89. Studies in anesthetized rats showed that renal pelvic administration of butaprost, 10 µM, and PGE2, 0.14 µM, resulted in similar ARNA responses, 1520±390 and 1170±270 %.sec (area under the curve of ARNA vs. time) that were blocked by DDA. Likewise, the ARNA response to increased renal pelvic pressure, 7180±710 %.sec, was blocked by DDA. Conclusion: PGE2 activates the cAMP-PKA pathway leading to a release of SP and activation of renal pelvic mechanosensory nerve fibers.
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