The forced oscillation and alveolar capsule techniques were applied to determine the input impedance of the lungs and the airway transfer impedances between 0.2 and 20 Hz in six open-chest dogs in the control state, during intravenous infusion of histamine at seven rates between 0.25 and 16 micrograms.kg-1.min-1, and after the infusion. In each condition, the input impedances seen from the alveolar capsules, i.e., terminal airway impedance (Zaw,ter), were measured by imposing 2- to 200-Hz oscillations from the capsules (B. L. K. Davey and J. H. T. Bates. Respir. Physiol. 91:165-182, 1993). Airway resistance (Raw) and inertance and tissue damping and elastance were derived from the lung impedance data. For all dogs, histamine progressively increased Raw and the real part of airway transfer impedance (airway transfer resistance), reaching, at 16 micrograms.kg-1.min-1, 241 +/- 109 (SD) and 370 +/- 186%, respectively, of the control value but caused greater, although locally highly variable, increases (769 +/- 716% of the control value) in the real part of Zaw,ter extrapolated to zero frequency (R0). With increasing doses of histamine, the changes in R0 always preceded those in Raw and airway transfer resistance implying that bronchoconstriction developed first in the lung periphery. It is therefore concluded that the measurement of Zaw,ter offers a sensitive method for the detection of early nonuniform responses to bronchoconstrictor stimuli that are not yet reflected by the values of the overall Raw. In one-half of the cases, significant increases in tissue damping and elastance occurred before any change in R0; this suggests that the mechanisms of airway and parenchymal constrictions may be unrelated.