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Inhibition of the Nicotinic Ion Channel by Arachidonic Acid and Other Unsaturated Fatty, Acids in Chromaffin Cells from Bovine Adrenal Medulla


 The effects of arachidonic and other cis-unsaturated fatty acids were investigated in cultured chromaffin cells from bovine adrenal medulla with respect to Ca2+ influx and secretion of catecholamines. As previously shown, arachidonic acid generated during the signal
 transduction is essential for the fusion of the chromaffin granules with the plasma membrane and by this enables secretion [10–12]. However, if one adds arachidonic acid externally before the agonist, this leads to a partial inhibition of the cholinergic induced secretion. Preincubation
 with cis-unsaturated fatty acids totally blocks the cholinergic induced Ca2+ influx but not the Ca2+ influx evoked by the voltage gated Ca2+ channel. This inhibition is not due to activation of protein kinase C by arachidonic acid, since preincubation
 with PMA does not block the receptor-dependent Ca2+ influx. Preincubation with 5-, 12, 15-HETE and 12-HPETE does not inhibit the receptor-dependent Ca2+ influx, indicating that eicosanoids are not responsible for the inhibition. This statement is supported by the fact
 that BW755C does not reverse the arachidonic acid-evoked blockade of the receptor-dependent Ca2+ influx. These results demonstrate that cis-unsaturated fatty acids and especially arachidonic acid inhibit the receptor-dependent Ca2+ influx by blocking the nicotinic
 cation channel. The generation of arachidonic acid in the physiological process of the stimulus-response coupling may, thus, contribute to the relaxation, of the cell by preventing further Ca2+ influx.
