Mechanism of stimulation of type J pulmonary receptors.

1. The responses of type J pulmonary receptors (identified according to existing criteria) were studied in anaesthetized cats by recording impulses in individual vagal afferent fibres whose conduction velocity ranged from 0.8 to 7 m/sec.2. Measurements of actual latencies between insufflation of halothane or ether into the lungs and the excitation of the endings, and the latencies before and after circulatory arrest have established that the endings are located in the interstitial tissues close to the pulmonary capillaries. Mainly for this reason, the term juxta-pulmonary capillary receptors (i.e. type J receptors) has been applied to these endings in preference to the term K deflation receptors used hitherto.3. The endings were stimulated by pulmonary congestion produced by occlusion of the aorta or left a-v junction for short periods. They were markedly stimulated during pulmonary congestion following injection of alloxan (150 mg/kg) or the addition of chlorine to the inspired air. This excitation was associated with a marked rise in pulmonary artery pressure and the occurrence of pulmonary oedema. However, the actual onset of excitation occurred some time after the rise in pressure and it was in fact more closely related to fall in pulmonary compliance. The frequency of discharge averaged over about 10-20 sec (in order to take the periods of relative inactivity into account) was 7.5 impulses/sec in 10 fibres (range 0.6-19 impulses/sec; S.D. 6.3). This is intense stimulation of the endings and the congestion so produced is therefore regarded as a severe stimulus for the endings.4. The pattern of excitation was variable. In some fibres the activity consisted of periodic bursts of impulses which seemed to be set off during the deflation phase of artificial respiration, sometimes during the inflation phase. This periodic activity was not due to contraction of smooth muscle as the endings are not stimulated following injection of histamine (into the right ventricle) which is known to stimulate smooth muscles in the alveolar ducts and respiratory bronchioles.5. It is postulated that the actual stimulus for the endings is a rise in interstitial pressure or volume produced by a rise in pulmonary capillary pressure. Evidence has been gathered to show that the latter rises during muscular exercise; this rise must stimulate the endings. It was therefore postulated that stimulation of the endings should cause reflex inhibition of limb muscles (for terminating exercise).