Hyperinflation in acute asthma has been associated with inspiratory muscle activity, which persist during expiration. The main objective of the present study was to evaluate the role of rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fibre endings in generating end-tidal inspiratory activity (ETIA).ETIA was induced by intravenous administration of histamine and continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. To differentiate between reflex activities from the three types of lung receptors, both vagus nerves were cooled to eight different temperatures (Tvg) between 4 and 37°C. It is known that CNAP stimulates RARs and inhibits SARs. Histamine was used to stimulate RARs, and this was combined with continuous positive airway pressure (CPAP) to further stimulate SARs.ETIA was evoked in the diaphragm and in parasternal intercostal muscles by both stimuli (histamine and CNAP) in 8 out of 18 cats. After vagotomy, neither histamine nor CNAP evoked ETIA any more. At Tvg=37°C, CPAP suppressed histamineinduced ETIA; whereas, this suppression was diminished at Tvg between 14 and 8°C. ETIA sharply declined for Tvg between 8° and 4°C, and at Tvg=4°C ETIA had virtually disappeared. At Tvg=37° and 22°C values of ETIA during CNAP were larger than those in response to histamine; whereas, at Tvg=10°C comparable ETIA values were obtained.It was shown that ETIA is a vagal reflex activity in which C-fibre endings are not involved. Histamine-induced ETIA originates from stimulation of RARs, and is inhibited by stimulation of SARs. Mechanical stimulation of RARs is a forceful stimulus to induce ETIA. This suggests that hyperinflation in acute asthma might be due, at least in part, to ETIA resulting from an imbalance between SAR and RAR activity. Eur Respir J., 1995Respir J., , 8, 2094Respir J., -2103 Bronchoconstriction and hyperinflation are characteristics of acute asthma [1]. Hyperinflation is considered to be disadvantageous to inspiratory muscle function, more so to the diaphragm than to the parasternal intercostal muscles (ICMs) [2]. Bronchoconstriction with an increased mechanical time constant and incomplete emptying of the lungs is one of the causes of hyperinflation [3]. Another factor is a persisting inspiratory muscle activity during expiration [4][5][6]. The electrical activity observed in the electromyogram (EMG) of inspiratory muscles at the end of expiration -just prior to the phasic increase in inspiratory activity -has been called tonic inspiratory activity [4,6]. As the origin of this so-called tonic activity is not yet clear, we prefer to use the term end-tidal inspiratory activity (ETIA). In asymptomatic asthmatics, it has been found that during histamine-induced hyperinflation the end-tidal pleural pressure was more negative than the predicted chest wall relaxation pressure at the corresponding end-tidal lung volume [4,5], indicating the presence of ETIA. In more direct measurements, by evaluating electromyograms (EMGs) of inspiratory...