Potassium does not mimic EDHF in rat mesenteric arteries

1 K+ has been proposed to be EDHF in small arteries. We compared ACh-stimulated. EDHF-mediated dilatation/relaxation with raised [K+], in rat mesenteric arteries. 2 In pressurized arteries, ACh (10 mu M) dilated all arteries. Raising [K+](o) from 5.88 to 10.58 mM only dilated 30% of arteries. Ba2+ (30 mu M) did not affect dilatation to ACh. but abolished 40% of dilatations to raised [K+](o). 3 If [K+](o) was lowered to 1.18 mM, restoring [K+](o) to 5.88 mM produced dilatation which was depressed by Ba2+ or ouabain (1 mM). Combined application of Ba2+ and ouabain abolished dilatation. In 1.18 mM K+, dilatation to ACh was depressed by ounbain, but not by Ba Combined application of Ba2+ and ouabain depressed dilatation further. Gap junction inhibitors (Gap-27; 300 mu M and 18-alpha-glycyrrhetinic acid; 100 mu M) also depressed dilatation to ACh. 4 In arteries mounted isometrically, ACh (1 mu M) relaxed endothelium intact (+ E). but not endothelium denuded (- E) arteries. Raising [K+](o) from 5.9 - 10.9 mM failed to relax all arteries. When [K+](o) was lowered to 1 mM, raising [K+](o) to 6 mM produced relaxation. in - E arteries, relaxation was unaffected by Ba2+ but abolished by ouabain. In + E arteries, Ba2+ depressed and ouabain abolished relaxation. In + E arteries, with 1 mM K+, ACh relaxation was depressed by ouabain but not Ba2+. The combined application of Ba2+ and ouabain further depressed relaxation. 5 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.