Rings of intrapulmonary bronchi isolated from rabbits producing anti-horseradish peroxidase IgE antibodies contracted when exposed to antigen. The contractile response had a lag period of about 1 min, reached a peak at 6 min and then subsided. Bronchi from rabbits with detectable levels of specific IgG (in addition to IgE) antibodies did not differ in response from those with undetectable specific IgG levels. Histamine also contracted rabbit intrapulmonary bronchi with an EC50 of 10ωM (SD 1.29). The response to antigen was completely inhibited with chlorpheniramine (30 ωM). In contrast to intrapulmonary bronchi, responsiveness of mainstem bronchi to antigen was observed only occasionally, whereas histamine was equipotent on both mainstem and intrapulmonary bronchi. Thus, the amount of antigen-induced mediator release may be less in the mainstem bronchi. Acetyl glyceryl ether phosphorylcholine, in concentrations up to 10 ωM, did not contract either mainstem or intrapulmonary bronchi. This study indicates that histamine is the major mediator of (and acetyl glyceryl ether phosphorylcholine does not significantly participate in) antigen-induced contraction of isolated bronchi from IgE-producing rabbits. The results provide a likely mechanism for the increase in pulmonary resistance observed in IgE anaphylaxis in this species.