RGD Reference Report - Activation of EP4 receptors contributes to prostaglandin E2-mediated stimulation of renal sensory nerves. - Rat Genome Database

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Activation of EP4 receptors contributes to prostaglandin E2-mediated stimulation of renal sensory nerves.

Authors: Kopp, UC  Cicha, MZ  Nakamura, K  Nusing, RM  Smith, LA  Hokfelt, T 
Citation: Kopp UC, etal., Am J Physiol Renal Physiol. 2004 Dec;287(6):F1269-82. Epub 2004 Aug 3.
RGD ID: 10003094
Pubmed: PMID:15292051   (View Abstract at PubMed)
DOI: DOI:10.1152/ajprenal.00230.2004   (Journal Full-text)

Induction of cyclooxygenase-2 (COX-2) in the renal pelvic wall increases prostaglandin E(2) (PGE(2)) leading to stimulation of cAMP production, which results in substance P (SP) release and activation of renal mechanosensory nerves. The subtype of PGE receptors involved, EP2 and/or EP4, was studied by immunohistochemistry and renal pelvic administration of agonists and antagonists of EP2 and EP4 receptors. EP4 receptor-like immunoreactivity (LI) was colocalized with calcitonin gene-related peptide (CGRP)-LI in dorsal root ganglia (DRGs) at Th(9)-L(1) and in nerve terminals in the renal pelvic wall. Th(9)-L(1) DRG neurons also contained EP3 receptor-LI and COX-2-LI, each of which was colocalized with CGRP-LI in some neurons. No renal pelvic nerves contained EP3 receptor-LI and only very few nerves COX-2-LI. The EP1/EP2 receptor antagonist AH-6809 (20 microM) had no effect on SP release produced by PGE(2) (0.14 microM) from an isolated rat renal pelvic wall preparation. However, the EP4 receptor antagonist L-161,982 (10 microM) blocked the SP release produced by the EP2/EP4 receptor agonist butaprost (10 microM) 12 +/- 2 vs. 2 +/- 1 and PGE(2), 9 +/- 1 vs. 1 +/- 0 pg/min. The SP release by butaprost and PGE(2) was similarly blocked by the EP4 receptor antagonist AH-23848 (30 microM). In anesthetized rats, the afferent renal nerve activity (ARNA) responses to butaprost 700 +/- 100 and PGE(2).780 +/- 100%.s (area under the curve of ARNA vs. time) were unaffected by renal pelvic perfusion with AH-6809. However, 1 microM L-161,982 and 10 microM AH-23848 blocked the ARNA responses to butaprost by 94 +/- 5 and 78 +/- 10%, respectively, and to PGE(2) by 74 +/- 16 and 74 +/- 11%, respectively. L-161,982 also blocked the ARNA response to increasing renal pelvic pressure 10 mmHg, 85 +/- 5%. In conclusion, PGE(2) increases renal pelvic release of SP and ARNA by activating EP4 receptors on renal sensory nerve fibers.



Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Ptger4Ratpositive regulation of substance P secretion, neurotransmission  IMP  RGD 

Cellular Component

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Ptger3Ratbrush border membrane  IDA  RGD 
Ptger4Ratneuron projection terminus  IDA  RGD 
Ptger4Ratneuronal cell body  IDA  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ptger3  (prostaglandin E receptor 3)
Ptger4  (prostaglandin E receptor 4)


Additional Information