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Phrenic nerve discharges were recorded as an output of respiratory activity in anaesthetized, vagotomized cats immobilized by gallamine and artificially ventilated with room air. 2. With the carotid sinus nerve (c.s.n.) intact or denervated, PcO2 threshold levels (Pth, CO2) were determined at arterial pH, varied between 7.0 and 7.6 ([H+] 25-100 nM) by successive intravenous infusions of 0.5 N-HCl or 1.0 M-NaHCO3. Ventilation was increased stepwise to induce a successive decrease in end-tidal PCO2. Pth, CO2 was defined as the level of end-tidal PCO2 at which phrenic discharges ceased. 3. With the c.s.n. intact, Pth, CO2 decreased linearly upon increasing arterial [H+]. The mean regression line, calculated from seven cats, was Pth, CO2 =-0.37 [H+] + 34.33. A similar inverse relationship was observed with the c.s.n. denervated. However, the slope of the regression line was significantly smaller, the mean regression line/eleven cats) being Pth,CO2 =-0.18 [H+]+ 35.06. 4. The relative contributions of arterial [H+] and PCO2 in stimulating the peripheral and central chemoreceptors could be estimated quantitatively. Arterial [H+] appears to be almost equally effective on both peripheral and central chemoreceptors; PCO2 acts exclusively on the central chemoreceptors. 5. Thus, the additive theory regarding the induction of respiratory activity by arterial [H+] and PCO2 was confirmed. In addition, the H+ drive was shown to be able to affect respiratory activity even in the absence of the peripheral chemoreceptors.