Potassium does not mimic EDHF in rat mesenteric arteries

K + has been proposed to be EDHF in small arteries. We compared ACh‐stimulated, EDHF‐mediated dilatation/relaxation with raised [K + ] o in rat mesenteric arteries. In pressurized arteries, ACh (10 μ M ) dilated all arteries. Raising [K + ] o from 5.88 to 10.58 m M only dilated 30% of arteries. Ba 2+ (30 μ M ) did not affect dilatation to ACh, but abolished 40% of dilatations to raised [K + ] o . If [K + ] o was lowered to 1.18 m M , restoring [K + ] o to 5.88 m M produced dilatation which was depressed by Ba 2+ or ouabain (1 m M ). Combined application of Ba 2+ and ouabain abolished dilatation. In 1.18 m M K + , dilatation to ACh was depressed by ouabain, but not by Ba 2+ . Combined application of Ba 2+ and ouabain depressed dilatation further. Gap junction inhibitors (Gap‐27; 300 μ M and 18‐α‐glycyrrhetinic acid; 100 μ M ) also depressed dilatation to ACh. In arteries mounted isometrically, ACh (1 μ M ) relaxed endothelium intact (+E), but not endothelium denuded (−E) arteries. Raising [K + ] o from 5.9–10.9 m M failed to relax all arteries. When [K + ] o was lowered to 1 m M , raising [K + ] o to 6 m M produced relaxation. In −E arteries, relaxation was unaffected by Ba 2+ but abolished by ouabain. In +E arteries, Ba 2+ depressed and ouabain abolished relaxation. In +E arteries, with 1 m M K + , ACh relaxation was depressed by ouabain but not Ba 2+ . The combined application of Ba 2+ and ouabain further depressed relaxation. In summary, both EDHF and raised [K + ] o dilate/relax rat mesenteric arteries, though sensitivities to barium and ouabain differ. K + may be a relaxing factor in this tissue, but its characteristics differ from EDHF. Gap junction inhibitors depress EDHF, implying an important role for myo‐endothelial gap junctions.British Journal of Pharmacology (2000) 130 , 1174–1182; doi: 10.1038/sj.bjp.0703412