Potassium ions and endothelium-derived hyperpolarizing factor in guinea-pig carotid and porcine coronary arteries

1 Experiments were designed to determine in two arteries (the guinea-pig carotid and the porcine coronary arteries) whether or not the endothelium-derived hyperpolarizing factor (EDHF) can be identified as potassium ions, and to determine whether or not the inwardly rectifying potassium current and the Na+/K+ pump are involved in the hyperpolarization mediated by EDHF. 2 The membrane potential of vascular smooth muscle cells was recorded with intracellular microelectrodes in the presence of N-omega-L-nitro-arginine (L-NA) and indomethacin. 3 In vascular smooth muscle cells of guinea-pig carotid and porcine coronary arteries, acetylcholine and bradykinin induced endothelium-dependent hyperpolarizations (-18+/-1mV, n = 39 and - 19 +/- 1 mV, n = 7, respectively). The hyperpolarizations were not affected significantly by ouabain (1 mu M), barium chloride (up to 100 mu M) or the combination of ouabain plus barium. 4 In both arteries, increasing extracellular potassium concentration by 5 or 10 mM induced either depolarization or in a very few cases small hyperpolarizations which never exceeded 2 mV. 5 In isolated smooth muscle cells of the guinea-pig carotid artery, patch-clamp experiments shows that only 20% of the vascular smooth muscle cells expressed inwardly rectifying potassium channels. The current density recorded was low (0.5+/-0.1 pA pF(-1), n = 8). 6 These results indicate that, in two different vascular preparations, barium sensitive-inwardly rectifying potassium conductance and the ouabain sensitive-Na+/K+ pump are not involved in the EDHF-mediated hyperpolarization. Furthermore, potassium did not mimic the effect of EDHF pointing out that potassium and EDHF are not the same entity in those arteries.