Cholinoceptor-mediated control of catecholamine release from chromaffin cells in the American eel, Anguilla rostrata.

The cholinergic agonist-induced secretion of catecholamines from chromaffin cells in the American eel, Anguilla rostrata, was assessed using a saline-perfused posterior cardinal vein preparation. Direct membrane depolarization with 60 mmol.l-1 K+ caused a significant release of catecholamines (adrenaline+noradrenaline) into the perfusate which was unaffected by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The nicotinic receptor agonist, 1,1-dimethyl-4-phenyl-piperazinium iodide, evoked catecholamine release in response to several doses exceeding 10(-7) mol; at 10(-5) mol the response was abolished by pre-treatment with the ganglion blocker, hexamethonium (final concentration = 10(-3) mol.l-1). The muscarinic receptor agonist, pilocarpine, did not elicit catecholamine release in response to any of the doses administered (10(-8)-10(-4) mol). A single injection of the mixed nicotinic/muscarinic cholinoceptor agonist, carbachol (10(-5) mol), caused the release of catecholamines which was abolished by pre-treatment with hexamethonium but which was unaffected by pre-treatment with the muscarinic receptor antagonist atropine (final concentration = 10(-5) mol.l-1). The results of this study indicate that the process of cholinergic agonist-induced catecholamine secretion from the chromaffin cells in the American eel is mediated exclusively by activation of nicotinic receptors with no involvement of the muscarinic receptor.