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Effects of hypoxia and dithionite on catecholamine release from isolated type I cells of the rat carotid body

1 Amperometric recordings were conducted to investigate the ability of hypoxia and anoxia to evoke quantal catecholamine secretion from isolated type I cells of the rat carotid body. 2 Hypoxia (P  O 2 8–14 mmHg) consistently failed to evoke catecholamine secretion from type I cells, when cells were perfused either at room temperature (21‐24 °C) or at 35–37 °C, and regardless of whether Hepes‐ or HCO3−/CO2‐buffered solutions were used. 3 Elevating extracellular [K+] caused concentration‐dependent secretion from individual type I cells, with a threshold concentration of approximately 25 mM. In the presence of this level of extracellular K+, hypoxia (P  O 2 8–14 mmHg) caused a marked enhancement of secretion which was fully blocked by 200 μM Cd2+, a non‐specific blocker of voltage‐gated Ca2+ channels. 4 Anoxia (N2‐equilibrated solution containing 0·5 mM dithionite) evoked exocytosis from type I cells when extracellular [K+] was 5 mM. This secretion was completely inhibited by removal of extracellular Ca2+, but was not significantly affected by Cd2+ (200 μM), Ni2+ (2 mM), Zn2+ (1 mM) or nifedipine (2 μM). Secretion was also observed when 0·5 mM dithionite was added to air‐equilibrated solutions. 5 Anoxia also evoked secretion from chemoreceptive phaeochromocytoma (PC12) cells, which was wholly Ca2+ dependent, but unaffected by Cd2+ (200 μM). 6 Our results suggest that hypoxia can evoke catecholamine secretion from isolated type I cells, but only in the presence of elevated extracellular [K+]. This may be due to the cells being relatively hyperpolarized following dissociation. In addition, we have shown that dithionite evokes catecholamine release regardless of P  O 2 levels, and this release is due mainly to an artefactual Ca2+ influx pathway activated in the presence of dithionite.