RGD Reference Report - Endothelin-B receptor activation triggers an endogenous analgesic cascade at sites of peripheral injury. - Rat Genome Database

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Endothelin-B receptor activation triggers an endogenous analgesic cascade at sites of peripheral injury.

Authors: Khodorova, A  Navarro, B  Jouaville, LS  Murphy, JE  Rice, FL  Mazurkiewicz, JE  Long-Woodward, D  Stoffel, M  Strichartz, GR  Yukhananov, R  Davar, G 
Citation: Khodorova A, etal., Nat Med. 2003 Aug;9(8):1055-61. Epub 2003 Jun 29.
RGD ID: 1581889
Pubmed: PMID:12847519   (View Abstract at PubMed)
DOI: DOI:10.1038/nm885   (Journal Full-text)

Endothelin-1 (ET-1) is a newly described pain mediator that is involved in the pathogenesis of pain states ranging from trauma to cancer. ET-1 is synthesized by keratinocytes in normal skin and is locally released after cutaneous injury. While it is able to trigger pain through its actions on endothelin-A (ET(A)) receptors of local nociceptors, it can coincidentally produce analgesia through endothelin-B (ET(B)) receptors. Here we map a new endogenous analgesic circuit, in which ET(B) receptor activation induces the release of beta-endorphin from keratinocytes and the activation of G-protein-coupled inwardly rectifying potassium channels (GIRKs, also named Kir-3) linked to opioid receptors on nociceptors. These results indicate the existence of an intrinsic feedback mechanism to control peripheral pain in skin, and establish keratinocytes as an ET(B) receptor-operated opioid pool.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
response to pain  IMP 1581889 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ednrb  (endothelin receptor type B)


Additional Information