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- W3016278142 abstract "The matching of red blood cell (RBC) supply to oxygen demand is an intricate process which requires generation of a capillary stimulus and triggering of a transduction process that dilates upstream arterioles. The sensor’s identity, the stimulus it generates and the mechanisms that enables it are openly debated and a source of active inquiry. This study tested whether extracellular K+ is the stimulus and if capillary KIR2.1 channels enable upstream arteriolar dilation via conduction. Experiments were performed in vivo, using a live microcirculatory preparation (extensor digitorum longus); the local oxygen environment was tightly controlled (custom stage insert) and capillary RBC kinetics monitored in mice lacking endothelial KIR2.1 or connexin 40. Dropping PO2 on the muscle surface (53 mmHg to 15 mmHg or 0 mmHg (3 min)) induced a stark microvascular response in control animals (RBC supply rate, velocity and hematocrit increased by 56%, 28% an 18%, respectively) without diminishing mitochondrial respiration. This blood flow response failed to materialize in connexin 40−/− mice. As this response was absent, capillary RBC O2 saturation was lower under normal conditions in the connexin 40−/− animals. In contrast, endothelial KIR2.1−/− mice reacted normally to O2 challenges, with RBC supply rate, velocity and hematocrit rising by 43%, 28%, and 11%, respectively. These findings show that coupling O2 demand-to-O2 supply requires coordinated electrical signaling among cells connected by gap junctions comprised of connexin 40. They also show that endothelial KIR2.1 channels are not responsible for initiating the hyperpolarization needed to drive conduction. These findings begin the process of restructuring our understanding of blood flow regulation and how O2 initiates this process independent of metabolite production. Support or Funding Information This work was funded by NSERC Discovery grants to CGE and to DGW." @default.
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- W3016278142 date "2020-04-01" @default.
- W3016278142 modified "2023-10-18" @default.
- W3016278142 title "Capillary Oxygen Triggers Conducted Hyperpolarization and Dilation Independent of Extracellular K + and Endothelial K IR 2.1" @default.
- W3016278142 doi "https://doi.org/10.1096/fasebj.2020.34.s1.04196" @default.
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