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Vol. 284, Issue 2, 549-552, February 1998
Laboratoire d'Anatomopathologie (N.N.) and
CNRS ERS 566 (I.G.,
C.L., J.P.G., X.N., C.B.) Centre Chirurgical Marie Lannelongue, Le
Plessis-Robinson, France
In human bronchial muscle preparations, nifedipine (3 µM)
significantly inhibited the histamine, ACh and KCl contractions. However, the dihydropyridine did not modify the contractile responses induced by either leukotriene D4 (LTD4) or
anti-human IgE (a-IgE). In human airways, SK&F 96365 (30 µM and 100 µM) markedly reduced the KCl and, at the higher concentration,
LTD4 maximal contractions. In addition, when preparations
were treated with nifedipine (3 µM), SK&F 96365 (100 µM)
significantly blocked responses to both LTD4 and a-IgE. The
calcium chelating agent ethylene glycol-bis (
-amino-ethyl ether)
N,N,N
,N
-tetraacetic acid (4 mM) also inhibited the a-IgE-induced
contractions. These data demonstrate that the nifedipine-resistant
component of the LTD4 and a-IgE contractions was inhibited
by SK&F 96365 and suggest that the cysteinyl-leukotriene receptor in
human airways may be intimately linked with a receptor-operated calcium-entry mechanism.
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