The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of oxygen sensitive potassium channels open at the resting membrane potential in pulmonary arteries smooth muscle cells (PASMCs), so the oxygen sensitive potassium channels in PASMCS play a vital role in the occurrence and development of hypoxic pulmonary vasoconstriction (HPV). Inhibition the function of channels by specific antagons, Antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, the O2 sensitivity of cloned K+ channels expressed in heterologous expression systems and gene targeting to knockout specific K+ channels have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive K+ channels. Although the mechanism of K+ channel inhibition by hypoxia is unknown, it appears that K+ α -subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or α-subunit. This review summarizes the role of K+ channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of K+ channel subunits involved in this response, and the possible mechanisms of K+ channel regulation by hypoxia. [
