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Contribution of nicotinic and muscarinic receptors in the secretion of catecholamines evoked by endogenous and exogenous acetylcholine

1983; Elsevier BV; Volume: 10; Issue: 3 Linguagem: Inglês

10.1016/0306-4522(83)90235-x

1873-7544

A R Wakade, Taruna D. Wakade,

Neurotransmitter Receptor Influence on Behavior

Abstract The aim of the present study was (1)to evaluate the functional contribution of nicotinic and muscarinic receptors of the rat adrenal medullary cells in the secretion of catecholamines evoked by exogenous and endogenous acetylcholine (2)to know whether the ratio of epinephrine to norepinephrine in the perfusate of the adrenal gland stimulated with various agents was comparable and close to that in the adrenal medulla (3)(3) to study the effect of tetrodbtoxin on the secretion of catecholamine evoked by nicotine and muscarine. Using nicotine and muscarine as agonists, and hexamethonium and atropine as antagonists, we found that the adrenal gland of the rat contains nicotinic and muscarinic receptors, and both are linked to the secretion of catecholamines. However, these receptors are activated in a different manner by endogenous and exogenous acetylcholine. Secretion evoked by injected acetylcholine was barely blocked by either hexamethonium or atropine, but their combination produced a block. In contrast, secretion evoked by endogenous acetylcholine (splanchnic nerve stimulation) was largely reduced (75%) by hexamethonium alone. The ratios of epinephrine to norepinephrine in the perfusate were comparable before and after stimulation of the adrenal gland with nicotine, acetylcholine, or K + ; the ratio was slightly higher for muscarine. Tetrodotoxin blocked the nicotine-evoked secretion by about 75% but had very little effect on the secretion evoked by muscarine. We suggest that nicotinic receptors are primarily concentrated in the synaptic zones and are involved in the physiological stimulation of the adrenal medulla, whereas extrasynaptic regions contain a mixture of nicotinic and muscarinic receptors, which are activated by injected acetylcholine. The tetrodotoxin experiments indicate that physiologically released acetylcholine can generate action potentials through synaptic nicotinic receptors to initiate increase in calcium influx and subsequent secretion of catecholamines.