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

E. Carpenter, C. J. Hatton * and C. Peers

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_O2 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_O2 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_O2 levels, and this release is due mainly to an artefactual Ca²⁺ influx pathway activated in the presence of dithionite.

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