Role of Carbon Dioxide for Hypoxic Chemotransduction of the Cat Carotid Body

Abstract

The interaction between hypoxia and hypercapnia in the genesis of increased neural activity from the carotid body has been appreciated for 30 year^2,3,4,7,8. When animals were hyperventilated, carotid chemoreceptor neural response to hypoxia was extremely reduced, and in some cases the response was almost abolished. On the other hand, the response of the carotid body to hypercapnia has never been abolished even under hyperoxic condition, although it is reduced. These observation has led us to hypothesize that the presence of carbon dioxide (CO₂) has some critical role for hypoxic chemotransduction of the carotid body. Because the carotid body is very sensitive to arterial CO₂ tension, and because CO₂/HCO₃ ^- is the main buffer in the biological system, regulation of intracellular pH (pHi) in the chemosensitive unit may exclusively depend on CO₂/HCO₃ ^- in vivo. Decrease in CO₂/HCO₃ ^- would increase pHi of the chemosensitive unit. Alkalinization of the unit would turn off the process of hypoxic chemotransduction. We tested this hypothesis using in vivo selective perfusion techniques of the carotid body. First, we examined the effect of the presence or absence of CO₂/HCO₃ ^- on the hypoxic chemotransduction of the carotid body. Second, we antagonized possible alkalinization of the chemosensitive unit during CO₂/HCO₃ ^--free perfusion by giving a non-volatile weak acid, butyrate. A part of this study has been reported previously ¹².