Studies were carried out to evaluate the mechanism by which neurotransmission through airway parasympathetic ganglia may be modulated during
immediate hypersensitivity reactions. Guinea pigs were passively sensitized by injection of guinea pig serum containing high-titer anti-
ovalbumin antibodies. Intracellular recordings were obtained from intrinsic parasympathetic ganglion neurons from the right mainstem bronchus in vitro.
Ovalbumin (10 micrograms/ml) elicited a membrane potential depolarization and changes in membrane resistance in bronchial
ganglion neurons from passively sensitized guinea pigs.
Histamine mimicked the depolarizing effect of
ovalbumin in a concentration-dependent manner (0.1-10 microM) and caused a transient increase and decrease in membrane resistance.
Pyrilamine, a
histamine H1-receptor antagonist, inhibited the
histamine-induced membrane depolarization and decrease in resistance. By contrast, blocking
histamine H2 and
H3 receptors did not inhibit
histamine-induced depolarization.
Pyrilamine also reduced the
antigen-induced depolarization of
ganglion neurons, demonstrating a role for
histamine H1 receptors in this response. The data provide evidence that the
antigen-induced depolarization of airway
ganglion neurons is secondary to an
antigen-antibody interaction on intrinsic mast cells and the consequential effect of
histamine on
H1 receptors. These studies demonstrate that
histamine released during an
immediate hypersensitivity reaction has direct effects on airway parasympathetic nerves.