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IgG-mediated anaphylactic contraction and 86Rb efflux from guinea pig tracheal smooth muscle.

Tracheal muscle strips isolated from guinea pigs passively sensitized with anti-egg albumin rabbit IgG were loaded with 86Rb as a K+ marker. The 86Rb efflux from the muscle tissue was measured after antigen exposure and the K(+)-channel subtypes involved in anaphylactic contraction were identified. The net 86Rb efflux was increased during antigen challenge. This increase was inhibited in Ca(2+)-free medium or in the medium of 40 mM of KCl, but not by 10 microM of glibenclamide or 20 mM of KCl. Decreased membrane potential and generation of action potentials were also observed during the anaphylactic contraction. As a comparison for antigen-induced 86Rb efflux changes, experiments using high concentrations of KCl were also performed. 86Rb efflux was increased depending on the KCl concentration. This increase was inhibited in Ca(2+)-free medium but not by 10 microM of glibenclamide. These results suggest that the K(+)-channel opening during IgG-mediated anaphylactic contraction was dependent on a decreased membrane potential due to 20-40 mM KCl. The subtype of the K(+)-channel involved is voltage-dependent K(+)-channel (Kv-channel), and Ca(2+)-activated K(+)-channel (KCa-channel) may also be involved in the 86Rb efflux change. The ATP-sensitive K(+)-channel (KATP-channel) was not involved in K(+)-channel opening during anaphylactic contraction.