Mechanisms underlying enhanced responses of J receptors of cats to excitants in pulmonary oedema.

1. The responses of J receptors to certain excitants were recorded during pulmonary oedema produced by phosgene gas (320-1080 p.p.m.) or alloxan, 150 mg kg-1 i.v., in cats anaesthetized with sodium pentobarbitone, 35 mg kg-1 I.P. 2. The responses of fourteen (out of fifteen) J receptors to phenyl diguanide (PDG) were greatly enhanced after phosgene, the enhancement being highly significant (P = < 0.01) in twenty-one out of twenty-six responses. The enhancements were also highly significant after alloxan in the case of another twelve receptors. Similar enhancements were observed in the case of responses to nicotine and capsaicin. This suggests that the enhancement of the responses of J receptors to excitants occurs in a non-specific manner after phosgene and alloxan. 3. The enhanced responses occurred in the absence of any significant increase in the estimated concentration of the excitants in pulmonary artery blood. 4. The enhanced responses to PDG were not closely related to the oedema-induced activity; several occurred during periods of silence of the receptors and in thirteen receptors the enhanced responses occurred before the increase in the oedema-induced activity had begun. 5. A possible role of histamine, 5-HT, prostaglandins and bradykinin in enhancing the responses to PDG after phosgene was excluded. 6. The results therefore suggest that the non-specific enhancement of the responses of the J receptors to excitants must be due to the increased permeability of the capillaries produced by phosgene and alloxan leading to greater movement of the excitants to the J receptors. However, certain unidentified factors may also be involved.