The membrane model of hypoxic transduction in chemoreceptor cells of the carotid body (CB) considers that voltage-operated channels play an important role in evoking the release of neurotransmitters in response to hypoxia. To some authors, maxi-K⁺ channels would contribute to control resting membrane potential in rat chemoreceptor cells (Wyatt et al. 1995), and thereby their hypoxic inhibition would depolarize the cells and trigger the release of neurotransmitters (Pardal et al. 2000); to some others maxi-K⁺ would serve to control electrical events in depolarized cells, setting, but not triggering, the magnitude of the release response (Pepper et al. 1995; Buckler, 1997). There are some authors, however, who consider maxi-K⁺ irrelevant to oxygen transduction (Donnelly, 1997; Lahiri et al. 1998). In rabbit chemoreceptor cells the available data imply that hypoxic inhibition of voltage-dependent transient potassium channels depolarizes the cells and triggers the hypoxic release response; or, in any case, it should be expected that voltage-dependent potassium channels would contribute to control electrical events in depolarized cells since in the hypoxic response in the rabbit cells tetrodotoxin-sensitive Na⁺ channels participate (Gonzalez et al. 1994).

Intact rat and rabbit carotid bodies (CB) were isolated under pentobarbital anaesthesia (40-60 mg kg^-1, I.P.). Animals were killed with an overdose of the anaesthetic. To study the release of [³H]catecholamines from chemoreceptor cells, CB catecholamine deposits were labelled by prior incubation of the organs with [³H]tyrosine. We have measured the release while incubating the CB in normoxic (P_O2 ~150 mmHg), hypoxic (10 min; P_O2 ~46 and ~23 mmHg) high K⁺ (10 min; 25 mM) and nicotine (10 min; 3 X 10^-4 M)-containing solutions in the absence of drugs and in the presence of tetraethylammonium (a blocker of maxi-K⁺ and transient K⁺ currents and a nicotinic antagonist; 1-10 mM) and iberiotoxin (a specific blocker of maxi-K⁺; 200 nM). In a few experiments we also used charybdotoxin (another maxi-K⁺ blocker, 10-50 nM).

We have found that tetraethylammonium (5 mM) reduced markedly the release of [³H]catecholamines induced by nicotine (97% in the rat and 93% in the rabbit), indicating that the blocker penetrates adequately in the intact CB. However, neither iberiotoxin nor tetraethylamonium altered the release of [³H]catecholamines in normoxia, suggesting that the channels sensitive to the blockers do not participate in the setting of resting membrane potential of chemoreceptor cells. During hypoxic stimulation tetraethylamonium (5 mM) did not alter the release induced by hypoxia in the rat CB, but it augmented the hypoxic response in the rabbit CB by a 43% (P < 0.05), indicating that tetraethylamonium-sensitive K⁺ channels play a role in setting of the magnitude of the hypoxic secretory response to hypoxia in the rabbit but not in the rat. The data suggest that in the rat tetraethylamonium-sensitive K⁺ channels are not strictly required for the repolarization of chemoreceptor cells after hypoxic depolarization.

This work was supported by Spanish DGICYT grants BFI2001-1713 and BFI2001-1691.