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(+)](o) in rat mesenteric arteries. 2. In pressurized arteries, ACh (10 microM) dilated all arteries. Raising [K(+)](o) from 5.88 to 10. 58 mM only dilated 30% of arteries. Ba(2+) (30 microM) 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 Ba(2+) or ouabain (1 mM). Combined application of Ba(2+) and ouabain abolished dilatation. In 1.18 mM 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 microM and 18-alpha-glycyrrhetinic acid; 100 microM) also depressed dilatation to ACh. 4. In arteries mounted isometrically, ACh (1 microM) 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 Ba(2+) but abolished by ouabain. In +E arteries, Ba(2+) depressed and ouabain abolished relaxation. In +E arteries, with 1 mM K(+), ACh relaxation was depressed by ouabain but not Ba(2+). The combined application of Ba(2+) 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.[1]References
- Potassium does not mimic EDHF in rat mesenteric arteries. Doughty, J.M., Boyle, J.P., Langton, P.D. Br. J. Pharmacol. (2000) [Pubmed]
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