Increased Function of Large‐Conductance of Potassium Channels following Acute Ischemic Stroke

We tested the hypothesis that acute ischemic stroke is associated with increased function of K + channels in vascular smooth muscle. Basilar smooth muscle from male rats was usedas a model. Animals underwent carotid surgery where a thin‐filament was inserted and guided to the bifurcation of the middle cerebral artery (MCA) from the internal carotid. The filament was then wedged to provide a transient occlusion of the MCA (MCAO) of sixtyminutes. Animals were then euthanized thirty days following MCAO. Whole‐cell patch clamp experiments indicated that K + current density was elevated in the stroke animals. Outward current density was 2.5 ± 0.2 fold greater in stroke animals. Ca 2+ ‐activated (BK) K + currents dominated membrane conductance at the more depolarized potentials. Paxilline (1 uM) a selective antagonist of BK channels was used to determine the contribution of these channels to the whole‐cell current. In control rats, paxilline inhibited 64 ± 2% of current at +80 mV. In stroke rats, paxilline inhibited 61 ± 3% of current at +80mV. The paxilline‐sensitive BK current was 2.4 ± 0.3 fold greater in stroke rats. These data indicate that acute ischemic stroke increases the expression or function of K channels invascular smooth muscle cells, especially BK channels. We suggest this change in K + channel function may represent a compensatory response aimed at preserving cerebral blood flow after ischemic stroke.