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Raising arterial potassium ([K+]a) from ca. 3.5 to 6.5 mM, as occurs in heavy exercise, excites the arterial chemoreceptors and ventilation (VE) in anaesthetised cats. We have previously shown that the excitation of chemoreceptors by potassium is enhanced by hypoxia and abolished by hyperoxia, and here we show, in decerebrate cats, that the potassium-induced increase in VE is also abolished by hyperoxia. 100% oxygen was given abruptly in hypoxia (PETO2 ca. 50 Torr), with inspired gas tensions adjusted to give the same PETO2 and PETCO2 values before all tests on a given animal. Intravenous infusions of 150 mM KCl, which raised [K+]a from 3.9 +/- 0.3 mM to 7.4 +/- 0.3 mM (mean +/- SE), always excited hypoxic VE (42 +/- 8%; P less than 0.01). Hyperoxia, given during KCl infusion, reduced VE to a value not significantly greater (P greater than 0.27) than the hyperoxic value obtained before infusion. These results show that: (i) VE reflects the responses of chemoreceptors to K+, (ii) that abrupt hyperoxia removes the potassium-induced ventilatory drive, and (iii) that, in our experiments, K+ appears to have excited VE only via the peripheral chemoreceptors.

Original publication




Journal article


Respir Physiol

Publication Date





223 - 230


Animals, Cats, Chemoreceptor Cells, Decerebrate State, Female, Infusions, Intravenous, Lung, Male, Oxygen, Physical Exertion, Potassium, Pulmonary Artery, Pulmonary Gas Exchange, Respiration