Pulmonary arteries constrict in response to hypoxia, a process thought to involve oxygen sensing by K+ channels. We therefore investigated the effects of hypoxia on voltage-activated K+ currents in myocytes isolated from rat small pulmonary arteries using the patch-clamp recording technique. Experiments with iberiotoxin and intracellularly applied Ca2+ chelating agents revealed that hypoxia (PO2, 20-30 mmHg; throughout) inhibited the Ca(2+)-insensitive component of the delayed voltage-activated outward K+ current. Hypoxia did not affect the membrane potential of these cells until they were depolarized by extracellular application of 20 mM K+, current injection or endothelin-1. Hypoxia caused little depolarization in the presence of prostaglandin F2 alpha, an agonist which was ineffective at inducing depolarization. These results suggest that an initial 'priming' depolarization may confer a sensitivity to hypoxia by activating delayed rectifier (Kv) channels. Once active, these channels can then be closed by hypoxia, leading to further depolarization. It is unlikely, therefore, that Kv channels are involved in controlling the resting membrane potential of these cells.

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