%0 Journal Article %A Don E. Griswold %A Stephen A. Douglas %A Lenox D. Martin %A T. Gregg Davis %A Laura Davis %A Zhaohui Ao %A Mark A. Luttmann %A Mark Pullen %A Ponnal Nambi %A Douglas W. P. Hay %A Eliot H. Ohlstein %T Endothelin B Receptor Modulates Inflammatory Pain and Cutaneous Inflammation %D 1999 %J Molecular Pharmacology %P 807-812 %V 56 %N 4 %X The role of endothelin B (ETB) receptors in inflammation and nociception was examined using ETB receptor knockout mice. Genotyping studies were used with tissues from ETB(+/+), ETB(+/−), and ETB(−/−) mice to confirm the loss of ETB receptors. Algesia induced by phenylbenzoquinone was evident in the (+/+) mice, reduced by ∼80% in the (+/−) mice, and absent in the (−/−) mice. Phenylbenzoquinone-induced algesia in (+/+) mice was inhibited 74% by the ETB receptor-selective antagonist A192621 (25 mg/kg p.o.), but unaffected by the ETA receptor-selective antagonist SB 234551 (25 mg/kg p.o.). Noninflammatory pain, induced by hotplate, was equivalent between (+/+) and (−/−) mice. The cutaneous inflammatory response to topical arachidonic acid (AA) also was evaluated. Whereas (+/+) mice had a marked inflammatory response to AA, the (+/−), and (−/−) mice had significantly reduced fluid phase responses (37 and 65% inhibition, respectively). Neutrophil infiltration also was reduced in the (+/−) and (−/−) mice (51 and 65% reduction, respectively). Topical administration of A192621 (500 μg/ear) in (+/+) mice inhibited AA-induced swelling (39%), whereas SB 234551 (500 μg/ear) was without effect. Collectively, these results implicate the ETB receptor in mediation of inflammatory pain and cutaneous inflammatory responses in mice. The American Society for Pharmacology and Experimental Therapeutics %U https://molpharm.aspetjournals.org/content/molpharm/56/4/807.full.pdf