Effects of potassium, oxygen and carbon dioxide on the steady-state discharge of cat carotid body chemoreceptors.
1. We have studied the effects of intravenous infusions of 0.1 mmol/min KCl (raising arterial potassium from ca. 3.2 to 6.0 mM) on the steady-state responses of carotid body chemoreceptors to end-tidal PCO2 and PO2 in the pentobarbitone-anaesthetized cat. 2. The excitatory effect of these KCl infusions was enhanced by hypoxia and reduced or abolished by hyperoxia. 3. Hypercapnia did not enhance, and usually reduced, excitation by KCl. 4. When similar control discharge frequencies were established by hypoxia or by hypercapnia, a KCl infusion excited the hypoxic discharge by about twice as much as it did the hypercapnic discharge. 5. These observations are not inconsistent with the idea that the mechanism underlying hypoxic excitation of arterial chemoreceptors is one that controls extracellular potassium concentration near the afferent nerve ending. 6. Insofar as potassium-induced excitation of chemoreceptor discharge is abruptly reduced by hyperoxia it behaves like Asmussen and Nielsen's postulated 'anaerobic work substance' and it may therefore contribute to the increased importance of the arterial chemoreflex reported in exercise.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002245:Carbon Dioxide / Q000502:physiology*; D002344:Carotid Body / Q000502:physiology*; D002415:Cats; D002628:Chemoreceptor Cells / Q000187:drug effects*; D010100:Oxygen / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology*; D013997:Time Factors
D002245:Carbon Dioxide; D011188:Potassium; D010100:Oxygen