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Vol. 56, Issue 2, 325-333, August 1999
Shift the Repertoire of Receptor Subtypes from B2
to B1 in Human Lung Fibroblasts
Department of Biochemistry, University of Texas Health Science
Center, San Antonio, Texas (S.B.P., L.M.F.L.-L.); and Division of
Endocrinology, National Institute for Biological Standards and Control,
South Mimms, Hertfordshire, United Kingdom (S.P.)
Elevated formation of bradykinin (BK) and Lys-BK or kallidin (KD) and
their carboxypeptidase metabolites desArg9BK and
desArg10KD is evident at sites of inflammation. Moreover,
B2 receptors (B2R), which mediate the action of BK and KD, participates
in the acute stage of the inflammatory and pain response, whereas B1
receptors (B1R), through which desArg9BK and
desArg10KD act, partake in the chronic stage. We
hypothesized that kinins autoregulate B2R and B1R expression in favor
of B1R. Incubation of IMR-90 cells with BK (100 nM) led to a loss
(89%) of B2R with a half-life (T1/2) of 7.0 min. Concomitantly, BK increased B1R (2- to 3-fold) with a
T1/2 of 120 min. DesArg10KD
(100 nM) had no effect on B2R but increased B1R (3- to 4-fold) with the
same rate as BK. Interleukin-1
(IL-1; 500 pg/ml) also increased
B1R (4- to 6-fold). Although both desArg10KD and BK
increased the level of IL-1 mRNA, IL-1 receptor antagonist inhibited the increase in B1R only in response to BK.
DesArg10KD and BK synergistically increased B1R (9-fold),
which was further increased by inclusion of IL-1 (36-fold).
Therefore, kinin metabolism and kinin-stimulated production of
cytokines may play a pivotal role in shifting the repertoire of kinin
receptor subtypes in favor of B1R during inflammation.
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