Abstract
Inwardly rectifying potassium channels (Kir) 2.x are expressed in cerebral endothelial cells (EC) but little is known about their role in vascular tone control. We tested the hypothesis that endothelial Kir amplify membrane hyperpolarization and cerebral vasodilation to ATP and UTP.MethodsExpression of Kir 2.1 and 2.2 was demonstrated in freshly isolated EC from rat middle cerebral artery (MCA) by PCR. Vasorelaxation (pressure myography) and endothelial hyperpolarization (di‐8‐ANEPPS) were measured in pressurized MCA following intraluminal delivery of UTP. Membrane current and voltage changes were recorded from mouse cerebral EC using perforated‐patch voltage clamp and current clamp techniques.ResultsUnstimulated EC showed Kir‐like (sensitive to Ba2+ and Kir 2.x blocker ML 133) and transient outward KCa‐like currents. Stimulation with ATP activated large outward currents that were sensitive to SKCa and IKCa blockers (UCL1684 and TRAM34). The ensuing membrane hyperpolarization was significantly attenuated in cells pretreated with Ba2+ or ML 133. In pressurized MCA, intraluminal application of Ba2+ significantly decreased hyperpolarization and relaxation responses to UTP.ConclusionEndothelial Kir2.x channels play a significant role in cerebral vasorelaxation by maintaining endothelial hyperpolarization in response to P2Y receptor stimulation. Supported by R01HL088435 to SPM
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