Preserved BK channel function in vasospastic myocytes from a dog model of subarachnoid hemorrhage

Cerebral vasospasm after subarachnoid hemorrhage (SAH) is due to contraction of smooth muscle cells in the cerebral arteries. The mechanism of this contraction, however, is not well understood. Smooth muscle contraction is regulated in part by membrane potential, which is determined by K+ conductance in smooth muscle. Voltage-gated (Kv) and large-conductance, Ca2+-activated K+ (BK) channels dominate arterial smooth muscle K+ conductance. Vasospastic smooth muscle cells are depolarized relative to normal cells, but whether this is due to altered Kv or BK channel function has not been determined. This study determined if BK channels are altered during vasospasm after SAH in dogs. We first characterized BK channels in basilar-artery smooth muscle using whole-cell patch clamping and single-channel recordings. Next, we compared BK channel function between normal and vasospastic cells. There were no significant differences between normal and vasospastic cells in BK current density, kinetics, Ca2+ and voltage sensitivity, single-channel conductance or apparent Ca2+ affinity. Basilar-artery myocytes had no, small- or intermediate-conductance, Ca2+-activated K+ channels. The lack of difference in BK channels between vasospastic and control cells suggests alteration(s) in other K+ channels or other ionic conductances may underlie the membrane depolarization and vasoconstriction observed during vasospasm after SAH.