Inhalation of furosemide, a loop diuretic, has shown favorable effects on experimentally induced cough, bronchoconstriction, and dyspnea. The effect of inhaled furosemide on tracheobronchial receptors was studied in anesthetized, spontaneously breathing rats. Single unit or pauci unit activity was recorded from the right vagus nerve. Tracheobronchial receptors were classified into slowly and rapidly adapting receptors (SARs and RARs, respectively), based on their adaptation index (AI), which was derived from the decrease in spike frequency (sf) over 2 s, expressed as a percentage of the peak firing rate. There were 43 SARs (AI </= 25%) and eight RARs (AI >/= 50%). Inhalation of furosemide (n = 29) increased the slope of airway pressure (Paw) versus sf of SARs from 8.6 to 14.8 Hz/cm H(2)O with an increase in sf at Paw = 0 cm H(2)O from 18.0 to 49.5 Hz, resulting in an upward shift of the line. Neither inhalation of vehicle (n = 9) nor intravenous injection of furosemide (n = 5) changed this relationship. In addition, inhalation of furosemide attenuated the activity of RARs. These findings indicate that SARs are sensitized and RARs desensitized by inhalation of furosemide. We discuss possible mechanisms for this, and its relevance to clinical problems of dyspnea, bronchoconstriction, and cough.