Apamin-Sensitive K + Currents Mediate Arachidonic Acid-Induced Relaxations of Rabbit Aorta

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Abstract
Arachidonic acid induces an endothelium-dependent relaxation of the rabbit aorta that is blocked by lipoxygenase inhibitors. The cellular vasodilatory mechanisms activated by arachidonic acid metabolites remain undefined. In rabbit thoracic aortic rings pretreated with indomethacin (10 μmol/L) and contracted with phenylephrine, arachidonic acid (0.1 to 100 μmol/L) induced concentration-dependent relaxations. Maximal relaxations averaged 45±3% and were inhibited by increasing extracellular K + (30 mmol/L, 15±5%; P P P 14 C]arachidonic acid metabolism. Whole-cell outward K + currents from isolated rabbit aortic smooth muscle cells averaged 43.0±4.8 pA/pF at 60 mV and were significantly decreased to 35.7±4.2 pA/pF by apamin ( P + current. In inside-out patches of aortic smooth muscle, apamin inhibited the calcium activation (100 to 300 nmol/L; P + channel (≈24 pS). These results suggest that arachidonic acid induces endothelium-dependent hyperpolarization and relaxation of rabbit aorta through activation of smooth muscle, apamin-sensitive K + currents.