Involvement of Na influx in acetylcholine receptor mediated secretion of catecholamines from cultured bovine adrenal medulla cells.
The role of sodium (Na) in stimulus-secretion coupling of adrenal medulla was investigated in primary culture of bovine adrenal medulla cells. In Na-free medium, the secretion of catecholamines and influx of 45Ca induced by carbachol were decreased to 30% and 18% of control responses, respectively. Carbachol induced secretion of catecholamines and influx of 45Ca were not inhibited by tetrodotoxin, a highly selective blocker of voltage dependent Na-channels. Carbachol caused a rapid influx of 22Na which was inhibited by hexamethonium but not by tetrodotoxin. Nicotine but not muscarine could be a substitute for carbachol and caused catecholamine secretion, 45Ca influx 22Na influx. Veratridine caused continuous secretion of catecholamines and influxes of 45Ca and 22Na which were blocked by tetrodotoxin. These results indicate that in cultured bovine adrenal medulla cells, stimulation of nicotinic receptor causes the influx of Na through receptor-mediated Na-channels but not through voltage-dependent Na-channels, and that influxed Na may facilitate the influx of Ca which triggers the secretory process. The sodium ion seems to be involved in the stimulus-secretion coupling evoked by physiological secretagogue in adrenal medulla.
D000313:Adrenal Medulla / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002395:Catecholamines / Q000378:metabolism*; D002417:Cattle; D002478:Cells, Cultured; D011950:Receptors, Cholinergic / Q000502:physiology*; D012964:Sodium / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D014701:Veratridine / Q000494:pharmacology
D002395:Catecholamines; D011950:Receptors, Cholinergic; D013779:Tetrodotoxin; D014701:Veratridine; D002217:Carbachol; D012964:Sodium