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The steady-state responses of respiration, measured as integrated phrenic nerve activity, to hypercapnic acidosis of the medullary extracellular fluid (e.c.f.) and to metabolically generated acidosis were compared in paralysed, vagotomized and glomectomized cats. E.c.f. hydrogen ion concentration [( H+]) was measured directly by means of a small (2 mm diameter) pH electrode placed on the ventral medulla. The results in ten cats show that changes of medullary e.c.f. [H+] were linearly related to changes of end-tidal PCO2 both before (r = 0.999) and after (r = 0.996) development of metabolic acidosis. There was a curvilinear relation between hypercapnic e.c.f. [H+] changes and the respiratory response that reflects progressive saturation of a central neural pathway between the chemoreceptors and the respiratory controller. This relation was similar in form both before and after development of metabolic acidosis. When acidosis of metabolic origin was present, apnea occurred with only small decreases of CO2 despite a high [H+]. The respiratory responses to the same e.c.f. [H+] change were only about one-half as large when they were generated metabolically as when they were generated by raising PCO2. Both exogenously induced metabolic acidosis (HCl infusion) and endogenous acidosis yielded similar results. We conclude that the e.c.f. [H+] does not represent the unique stimulus to the central chemoreceptors. We discuss several alternate mechanisms for the action of CO2 and [H+] on central chemoreceptors but none can be considered definitive at the present time.

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