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Vol. 56, Issue 4, 807-812, October 1999
Departments of Pulmonary Pharmacology (D.E.G., L.D.M., M.A.L.,
D.W.P.H.), Cardiovascular Pharmacology (S.A.D., Z.A., E.H.O.),
Immunology (T.G.D.), Laboratory Animal Science (L.D.), and Renal
Pharmacology (M.P., P.N.), SmithKline Beecham Pharmaceuticals, King of
Prussia, Pennsylvania
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.
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