Hypoxia-induced pulmonary vasoconstriction involves the inhibition of voltage-gated K+ channels, likely through interaction with an unidentified O2 sensor or beta-subunit rather than direct sensing.
The review outlines the molecular components of O2-sensitive KV channels in pulmonary arteries, providing mechanistic insights into hypoxia-induced pulmonary vasoconstriction.
The hypoxia-induced membrane depolarization and subsequent constriction of small resistance pulmonary arteries occurs, in part, via inhibition of vascular smooth muscle cell voltage-gated K+ (KV) channels open at the resting membrane potential. Pulmonary arterial smooth muscle cell KV channel expression, antibody-based dissection of the pulmonary arterial smooth muscle cell K+ current, and the O2 sensitivity of cloned KV channels expressed in heterologous expression systems have all been examined to identify the molecular components of the pulmonary arterial O2-sensitive KV current. Likely components include Kv2.1/Kv9.3 and Kv1.2/Kv1.5 heteromeric channels and the Kv3.1b alpha-subunit. Although the mechanism of KV channel inhibition by hypoxia is unknown, it appears that KV alpha-subunits do not sense O2 directly. Rather, they are most likely inhibited through interaction with an unidentified O2 sensor and/or beta-subunit. This review summarizes the role of KV channels in hypoxic pulmonary vasoconstriction, the recent progress toward the identification of KV channel subunits involved in this response, and the possible mechanisms of KV channel regulation by hypoxia.
Coppock et al. (Sun,) conducted a review in Hypoxia-induced pulmonary vasoconstriction. Hypoxia was evaluated. Hypoxia-induced pulmonary vasoconstriction involves the inhibition of voltage-gated K+ channels, likely through interaction with an unidentified O2 sensor or beta-subunit rather than direct sensing.