Carbon Dioxide — Essential Ingredient for in vivo Carotid Body Chemotransduction

Abstract

The carotid body responds to the changes in arterial Po₂, Pco₂, and pH. Although different mechanisms have been suggested for the chemotransduction of hypoxia and hypercapnia in the carotid body, it is also true that the response of the carotid body to one stimuli is not totally independent of other stimuli. Several studies have shown that lowering arterial Pco₂ can dramatically reduce the carotid body response to hypoxia^{2, 3, 4, 5}. In addition, we have recently demonstrated that, whereas selective perfusion of the carotid body with hypoxic perfusate containing CO₂/HCO₃ ^- increased carotid chemoreceptor neural activity, perfusion with CO₂/HCO₃ ^--free hypoxic perfusate did not This suggested a crucial role for CO₂/HCO₃ ^- in hypoxic chemotransduction⁷. Pertinent to these studies a recent report showed that intracellular pH of the type I cell from the rat carotid body was very alkalotic in the CO₂/HCO₃ ^--free media¹. Based on these findings we hypothesized that CO₂/HCO₃ ^- plays a fundamental role for the carotid body chemotransduction, possibly as an essential ingredient in the regulatory mechanisms of intracellular pH (pH/) in the chemosensitive unit. Decrease in CO₂/HCO₃ ^- would increase pH/ of the chemosensitive unit. Alkalinization of the unit would turn off the process of chemotransduction. We tested this hypothesis using a technique of in vivo selective perfusion of the carotid body.