Abstract

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 (β-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.