Potential role of H 2O 2 in chemoreception in the cat carotid body

Abstract

The hypothesis that H 2O 2 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 O 2 ( P tiO 2 ). According to the hypothesis NADPH mediated, P O 2 dependant increase in H 2O 2 production would hyperpolarize the glomus cell, decreasing the chemosensory discharge. Thus, lactate and aminotriazole which would increase H 2O 2 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 tiO 2 . Diethyldithiocarbamic acid (5 mM), which blocks the conversion of superoxide to H 2O 2, also diminished the chemosensory discharge, presumably due to an increased CB P tiO 2 . Menadione (increasing H 2O 2) and t-butyl hydroperoxide irreversibly decreased the chemosensory discharge, and the data are not useful. H 2O 2 increased the P O 2 of the perfusate, and therefore could not be tested against P O 2 . Thus, perturbation of endogenous or exogenous H 2O 2 did not provide any evidence for its critical role in O 2 chemoreception.