ATP Content in the Cat Carotid Body under Different Experimental Conditions. Support for the Metabolic Hypothesis

Abstract

As early as 1931 it was demonstrated by Heyman’s group that the dyspnoeic effect of cyanide was reflexly mediated: the origin of the reflex was located in the area of the carotid sinus and it was also demonstrated that the reflex disappeared after sectioning the carotid sinus nerve (CSN). In the following three decades pari-pasu to the discovery of the metabolic pathways of general metabolism and the description of metabolic blockers or metabolic poisons, it was shown, principally by the Russian school, that all metabolic poisons stimulated respiration. These and other findings culminated in 1963 with the proposal of the metabolic hypothesis of chemoreception (see Anichkov and Belenkii, 1963). Torrance (1968) in summarizing the most relevant literature on the arterial chemoreceptors, reformulated clearly the metabolic hypothesis as it is presented in Figure 1. The idea of a hypoxic sensory transmitter seemed to be accepted at the end of the Oxford Symposium: it emerged also from the same symposium the idea of a dual transduction mechanism in the carotid body (CB): one for hypoxia (the metabolic hypothesis) and other for CO₂-low pH by non defined pathways (Krylov and Anichkov 1968). With ups and downs the metabolic hypothesis has survived until the eighties when Lahiri’s group (Mulligan et al 1981, Erhan et al. 1981) revitalized the metabolic hypothesis emphasizing again the duality of transduction mechanisms for hypoxia and high CO₂-low pH (see also Lahiri et al. 1982, Lahiri, 1984 and Fitzgerald and Dehghani 1982) in opposition to the unitary mechanism proposed by Torrance and coworkers (Torrance 1974, 1977, Hanson et al. 1981).