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http://purl.uniprot.org/citations/15838353http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15838353http://www.w3.org/2000/01/rdf-schema#comment"In some diseases in which endothelin-1 (ET-1) production increases (e.g. prostate cancer), ET-1 is considered to be involved in the generation of pain. In the present study, we investigated the effects of a selective endothelin-A receptor antagonist, YM598, on the nociception potentiated by ET-1 in formalin-induced and cancer inoculation-induced pain models in mice. The formalin-induced pain model was prepared by intraplantar injection of 0.7% formalin into the hind paws of ICR mice, and the cancer pain model was prepared by inoculation of the human prostate cancer cell line PPC-1 into the hind paws of severe combined immunodeficiency mice. Formalin caused a biphasic pain response and paw edema in the mouse hind paw. ET-1 (10 pmol/paw) potentiated these responses, and single oral administration of YM598 (0.3-3 mg/kg) significantly inhibited this ET-1-induced potentiation of nociception and paw edema. ET-1 (10 pmol/paw) also potentiated the pain response in prostate cancer-inoculated mice. Both YM598 and atrasentan (0.3-3 mg/kg) significantly inhibited the ET-1-induced potentiation of nociception. These results suggest that selective endothelin-A receptor antagonists relieve pain in patients with various diseases in which ET-1 production increases (e.g. prostate cancer)."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.org/dc/terms/identifier"doi:10.1097/01.fjc.0000166309.63808.5f"xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Miyata K."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Sato S."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Tanaka S."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Shibasaki K."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Fujimori A."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Sudoh K."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Sasamata M."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Fujiyasu N."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Koakutsu A."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/author"Yuyama H."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/name"J Cardiovasc Pharmacol 44 Suppl"xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/pages"S479-82"xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/title"Inhibitory effects of a selective endothelin-A receptor antagonist YM598 on endothelin-1-induced potentiation of nociception in formalin-induced and prostate cancer-induced pain models in mice."xsd:string
http://purl.uniprot.org/citations/15838353http://purl.uniprot.org/core/volume"1"xsd:string
http://purl.uniprot.org/citations/15838353http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15838353
http://purl.uniprot.org/citations/15838353http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15838353
http://purl.uniprot.org/uniprot/#_P22387-mappedCitation-15838353http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15838353
http://purl.uniprot.org/uniprot/#_Q61614-mappedCitation-15838353http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15838353
http://purl.uniprot.org/uniprot/#_Q544E0-mappedCitation-15838353http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15838353
http://purl.uniprot.org/uniprot/#_Q8BMW4-mappedCitation-15838353http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15838353
http://purl.uniprot.org/uniprot/P22387http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15838353