| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Departments of Internal Medicine and Pharmacology, Department of Veterans Affairs, Medical Center, and University of Iowa Roy J. and Lucille Carver College of Medicine, Iowa City, Iowa 52242
Submitted 11 November 2002 ; accepted in final form 6 May 2003
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 a low- and enhanced by a high-sodium (Na+) diet, suggesting an inhibitory effect of ANG. We now examined whether 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 a low- and high-Na+ diet, respectively. In a renal pelvic preparation from high-Na+-diet rats, 0.14 µM PGE2 produced an increase in SP release from 7 ± 1 to 19 ± 3 pg/min that 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 analog 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- 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, 1,670 ± 490 and 1,760 ± 400%·s (area under the curve of ARNA vs. time). Similarly, the ARNA responses to increases in renal pelvic pressure were similarly enhanced by CPT-cAMP in normal- and low-Na+-diet rats. In 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.
afferent renal nerves; high-sodium diet; low-sodium diet; pertussis toxin; Gi protein; bradykinin
This article has been cited by other articles:
|
|
 |
|
  M. R. Quinlan, N. G. Docherty, R. W. G. Watson, and J. M. Fitzpatrick Exploring mechanisms involved in renal tubular sensing of mechanical stretch following ureteric obstruction Am J Physiol Renal Physiol, July 1, 2008; 295(1): F1 - F11. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. C. Kopp, M. Z. Cicha, and M. A. Yorek Impaired responsiveness of renal sensory nerves in streptozotocin-treated rats and obese Zucker diabetic fatty rats: role of angiotensin Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2008; 294(3): R858 - R866. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. C. Kopp, M. Z. Cicha, and L. A. Smith Differential effects of endothelin on activation of renal mechanosensory nerves: stimulatory in high-sodium diet and inhibitory in low-sodium diet Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2006; 291(5): R1545 - R1556. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. C. Kopp and M. Z. Cicha Impaired substance P release from renal sensory nerves in SHR involves a pertussis toxin-sensitive mechanism Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2004; 286(2): R326 - R333. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
