Gap junctions and the transfer of reactive oxygen species during endothelium‐dependent contractions

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To assess whether or not reactive oxygen species (ROS) and gap junctions contribute to endothelium‐dependent contractions in the aorta of spontaneously hypertensive rats (SHR), rings with or without endothelium, treated with antioxidants or gap junction inhibitors, were studied by recording of isometric force. Superoxide dismutase and catalase did not affect, while diethyldithiocarbamate or manganese (III) tetrakis(1‐methyl‐4‐pyridyl)porphyrin (cell permeable antioxidants) reduced endothelium‐dependent contractions to acetylcholine and the calcium ionophore A23187. The gap junction inhibitors, 18β‐ glycyrrhetinic acid and carbenoxolone also reduced these contractions. The gap peptides 40Gap27, 37,43Gap27 and 43Gap26 decreased responses to acetylcholine, but only 40Gap27 reduced those to A23187. These findings suggest that ROS contribute to endothelium‐dependent contractions in the SHR aorta. Myoendothelial gap junctions permit the transfer of ROS, explaining why the response is uninterrupted by antioxidants with poor cell permeability but are sensitive to antioxidants with high permeability. The endothelium‐dependent contraction to acetylcholine involves connexins 37, 40 and 43, while only connexin 40 is involved in that to A23187. This study is supported by the RGC of HKU.