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Department of Internal Medicine, Department of Veterans Affairs Medical Center, Iowa City 52246; and University of Iowa College of Medicine, Iowa City, Iowa 52242
Increasing renal pelvic pressure increases afferent renal nerve activity (ARNA) by a 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 subthreshold 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, 1,520 ± 390 and 1,170 ± 270% · s (area under the curve of ARNA vs. time) that were blocked by DDA. Likewise, the ARNA response to increased renal pelvic pressure, 7,180 ± 710% · s, was blocked by DDA. In conclusion, PGE2 activates the cAMP-PKA pathway leading to a release of SP and activation of renal pelvic mechanosensory nerve fibers.
afferent renal nerves; EP2 receptors; calcitonin gene-related peptide; kidney; forskolin; adenylyl cyclase; protein kinase A; mechanosensory nerves
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