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O₂-sensitive K⁺ channels in immortalised rat chromaffin-cell-derived MAH cells

Ian M. Fearon*, Roger J. Thompson*, Imtiaz Samjoo*, Cathy Vollmer*, Laurie C. Doering† and Colin A. Nurse*

The regulation of K⁺ channels by O₂ levels is a key link between hypoxia and neurotransmitter release in neuroendocrine cells. Here, we examined the effects of hypoxia on K⁺ channels in the immortalised v-myc, adrenal-derived HNK1⁺ (MAH) cell line. MAH cells possess a K⁺ conductance that is sensitive to Cd²⁺, iberiotoxin and apamin, and which is inhibited by ~24 % when exposed to a hypoxic perfusate (O₂ tension 20 mmHg). This conductance was attributed to high-conductance Ca²⁺-activated K⁺ (BK) and small-conductance Ca²⁺-activated K⁺ (SK) channels, which are major contributors to the O₂-sensitive K⁺ conductance in adrenomedullary chromaffin cells. Under low [Ca²⁺]_i conditions that prevented activation of Ca²⁺-dependent K⁺ conductances, a rapidly activating and slowly inactivating K⁺ conductance, sensitive to both TEA and 4-aminopyridine (4-AP), but insensitive to 100 nM charybdotoxin (CTX), was identified. This current was also reduced (by ~25 %) when exposed to hypoxia. The hypoxia-sensitive component of this current was greatly attenuated by 10 mM 4-AP, but was only slightly reduced by 10 mM TEA. This suggests the presence of delayed-rectifier O₂-sensitive channels comprising homomultimeric Kv1.5 or heteromultimeric Kv1.5/Kv1.2 channel subunits. The presence of both Kv1.5 and Kv1.2 -subunits was confirmed using immunocytochemical techniques. We also demonstrated that these K⁺ channel subunits are present in neonatal rat adrenomedullary chromaffin cells in situ. These data indicate that MAH cells possess O₂-sensitive K⁺ channels with characteristics similar to those observed previously in isolated chromaffin cells, and therefore provide an excellent model for examining the cellular mechanisms of O₂ sensing in adrenomedullary chromaffin cells.

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