Nicotine stimulates secretion of both catecholamines and acetylcholinesterase from cultured adrenal chromaffin cells.
There is conflicting evidence from studies on sympathetic ganglia and the adrenal medulla concerning the morphological and biochemical localization and physiological role(s) of the enzyme acetylcholinesterase (AChE). Furthermore, the origin of the AChE released from the adrenal medulla (whether from chromaffin cells or splanchnic nerve, or both) has not been firmly established. We have examined the efficacy of cholinergic agonists to release endogenous AChE and catecholamines (CA) from monolayer cultures of purified bovine adrenal chromaffin cells. The nicotinic agonist (nicotine), but not the muscarinic agonist (methacholine), released both AChE and CA from the adrenal chromaffin cells. The concomitant release of CA and AChE evoked by nicotine was Ca++ dependent with a correlation coefficient r = 0.82 (p less than 0.001). The results show that adrenal chromaffin cells in vitro, a system free of splanchnic nerve elements, can still release AChE. The finding that concomitant release of AChE and catecholamines occurs on exposure of the cells to nicotinic agonists suggests that released AChE may have a physiological role at neuroeffector junctions.[1]References
- Nicotine stimulates secretion of both catecholamines and acetylcholinesterase from cultured adrenal chromaffin cells. Mizobe, F., Livett, B.G. J. Neurosci. (1983) [Pubmed]
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