Bradykinin stimulates afferent vagal C-fibers in intrapulmonary airways of dogs.

Bradykinin is released in the lungs in asthma and pulmonary anaphylaxis. It has negligible direct bronchoconstrictor effects in humans or dogs, but inhaled as aerosol it causes cough and reflex bronchoconstriction in asthmatics and some normal subjects. The afferent nerves responsible for these reflex effects have not been identified. We recorded vagal impulses in anesthetized dogs to determine whether lung afferents were stimulated by bradykinin. C-fiber endings in the intrapulmonary airways accessible from the systemic circulation were stimulated by bradykinin injected into the left atrium (0.5-1.0 micrograms/kg) or bronchial artery (1.5 micrograms), activity increasing 15-fold on average. C-fiber endings accessible from the pulmonary circulation were relatively insensitive to bradykinin. Bradykinin caused a small increase in firing of some rapidly adapting (irritant) receptors, but the effect appeared to be secondary to vascular changes. Bradykinin had variable effects on slowly adapting stretch receptors, but did not stimulate them directly. Thus vagally mediated sensory or reflex effects initiated by bradykinin in the lung are probably due to stimulation of "bronchial" C-fibers.