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1 Department of Veterans Affairs Medical Center, Iowa City, IA, USA
2 Departments of Internal Medicine and Pharmacology, University of Iowa Roy J. and Lucille Carver College of Medicine, Iowa City, IA, USA
* To whom correspondence should be addressed. E-mail: ukopp{at}blue.weeg.iuowa.edu.
Activation of renal sensory nerves involves PGE2-mediated release of substance P (SP) via activation of the cAMP-PKA pathway. The PGE2-mediated SP release is suppressed by low and enhanced by high sodium (Na+) diet suggesting an inhibitory effect of angiotensin (ANG). We now examined if ANG II is present in the pelvic wall and inhibits PGE2-mediated SP release by blocking PGE2-mediated increases in cAMP. ANG II levels in renal pelvic tissue were 710±95 and 260±30 fmol/g tissue in rats fed low and high Na+ diet. In a renal pelvic preparation from high Na+ diet rats, 0.14 µM PGE2 increased SP release from 7±1 to 19±3 pg/min which was blocked by 15 nM ANG II. Treating pelvises with pertussis toxin (PTX) abolished the effects of ANG II. In pelvises from low Na+ rats, neither basal nor bradykinin-mediated SP release was altered by PGE2. However, the bradykinin-mediated release of SP was enhanced by the permeable cAMP analogue CPT-cAMP, from 4±1 to 11±2 pg/min, a response similar to that in normal Na+ diet rats. In vivo, renal pelvic administration of PGE2 enhanced the afferent renal nerve activity (ARNA) response to bradykinin in normal Na+ diet rats, but not in low Na+ diet rats. CPT-cAMP produced similar enhancement of the ARNA responses to bradykinin in normal and low Na+ diet rats, 1670±490 and 1760±400 % .sec (area under the curve of ARNA vs. time). Likewise, the ARNA responses to increases in renal pelvic pressure were similarly enhanced by CPT-cAMP in normal and low Na+ diet rats. Conclusion, renal pelvic ANG II modulates the responsiveness of renal sensory nerves by suppressing PGE2-mediated activation of adenylyl cyclase via a PTX-sensitive mechanism.
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