In cats anaesthetized with a mixture of chloralose and urethane, stimulation of pulmonary C fibres by right atrial injections of phenylbiguanide caused, after a latency of about 3 s, a reduction in pulmonary ventilation or apnoea, bradycardia and systemic hypotension, confirming previous work. 2. A decrease in femoral artery perfusion pressure also occurred under conditions in which the hindlimb was vascularly isolated, the blood flow was maintained constant and the inferior vena caval pressure did not change. This indicates a reduction in vascular resistance due to vasodilatation. The response was unaffected by atropine and propranolol, but was reduced or abolished by guanethidine, hexamethonium and denervation of the limb, indicating that it is due to a reduction in activity in sympathetic vasoconstrictor fibres. 3. Similar cardiovascular responses were observed when the arterial blood pressure was maintained constant, and also in artificially ventilated animals. 4. Evidence is presented that the receptors responsible for the respiratory and cardiovascular responses to right atrial injections of phenylbiguanide lie in the pulmonary vascular bed. 5. When the pulmonary C fibres were excited during a period of apnoea which was induced reflexly by electrical stimulation of the central end of a superior laryngeal nerve, there were no consistent differences in the size of the cardiac or vascular responses compared to the control responses in the absence of the laryngeal input. This result occurred irrespective of the size of the control ventilatory response to phenylbiguanide. 6. By contrast in the same experiments, the cardio-inhibitory and vasoconstrictor responses to excitation of the carotid body chemoreceptors were invariably potentiated by electrical stimulation of a superior laryngeal nerve, as found previously. 7. The possible central mechanisms responsible for the differential modulation of pulmonary C fibre and carotid chemoreceptor reflexes by respiration are discussed.
