This report represents a relevant contribution to the study of oxygen sensing for two main reasons. First, it shows an approach adequate for identification of a putative O2-sensitive K+ channel, by moving from the modulation by hypoxia of a recombinant channel back to its physiological context, the role of this channel in the response to low Po2 of the native cells. Second, it demonstrates that hypoxic inhibition of the recombinant Kv3.1 channels is retained in excised membrane patches, pointing to a membrane-delimited mechanism as the origin of hypoxic responses. The importance of this latter finding deserves additional comment.
