Potential role of H2O2 in chemoreception in the cat carotid body

The hypothesis that H2O2 plays a critical role in hypoxic chemoreception in the cat carotid body (CB) was tested using a perfused-superfused preparation in vitro, measuring chemosensory discharge and CB tissue P-O2 (P-tiO2). According to the hypothesis NADPH mediated, P-O2 dependant increase in H2O2 production would hyperpolarize the glomus cell, decreasing the chemosensory discharge. Thus, lactate and aminotriazole which would increase H2O2 concentration, would decrease the chemosensory discharge during hypoxia. However, 2.5-5.0 mM lactate and 25 mM aminotriazole did not diminish the hypoxic response. But, 2.5 mM lactate decreased the chemosensory discharge during normoxia which can be explained by an increase of CB P-tiO2. Diethyldithiocarbamic acid (5 mM), which blocks the conversion of superoxide to H2O2, also diminished the chemosensory discharge, presumably due to an increased CB P-tiO2. Menadione (increasing H2O2) and t-butyl hydroperoxide irreversibly decreased the chemosensory discharge, and the data are not useful. H2O2 increased the P-O2 Of the perfusate, and therefore could not be tested against P-O2 Thus, perturbation of endogenous or exogenous H2O2 did not provide any evidence for its critical role in O-2 chemoreception.