Role of Ion-Exchangers in the Cat Carotid Body Chemotransduction

Abstract

CO₂-O₂ stimulus interaction in the responses of the carotid body (CB) chemosensory discharges is well known ^I. Consistent with this is the observation that the response to hypoxia can be eliminated by diminishing the strength of CO₂ stimulus ². On the other hand, PCO₂ and H⁺ stimuli can elicit a response without tissue hypoxia. Accordingly it may be hypothesized that the hypoxic response is based on and mediated by the CO₂- dependent fr stimulus. The hypothesis, however, cannot be fully tested in vivo because CO₂ cannot be eliminated to study the effects of hypoxia alone. In vitro experiments offers the advantage that CO₂-HCO₃ ^- can be eliminated in the external milieu, and the extracellular [H⁺] can be manipulated to test the idea that hypoxic response is dependent on CO₂-HCO₃ ^- and is mediated by cellular [H⁺].The current proposal is that decreases in glomus cell pH or PO₂ initiate intracellular Ca²⁺ changes, perhaps preceded by its membrane responses and followed by the release of neurotransmitters which, acting on the respective receptors, lead to neural chemosensory discharges¹. If the chemosensory responses are determined by events in the glomus cells, several predictions can be made and tested regarding chemoreception in these cells.