抄録
The actions of nicotinic receptor agonists and antagonists on Ca movement in perfused bovine adrenal glands were investigated. 1, 1 -dimethyl-4-phenylpiperazinium (DMPP, 0.3 mM) and acetylcholine (ACh, 0.3 mM, containing 10 μM physostigmine) produced a significant increase in 45Ca efflux from 45Ca preloaded adrenal glands and which was closely correlated with an increase of adrenal catecholamine (CA) secretion. In the perfused adrenal glands which the stimulation of 45Ca efflux as well as adrenal CA secretion by ACh was abolished in Ca free Locke's solution, the application of Ca (22 mM) considerably restored the stimulatory response of 45Ca efflux to ACh. There was a significant increase in the 45Ca uptake by nicotinic agonists-stimulated adrenal glands, which was responsible for the enhancement of Ca uptake by adrenal medulla and not by the cortex. The maximal increase in 45Ca uptake by nicotinic agonists preceded that in the adrenal CA secretion. Nicotinic antagonists such as surugatoxin (SGTX, 20 μM) and mecamylamine (0.1 mM) markedly (60-90%) reduced the stimulation of uptake and efflux of 45Ca by the agonists. Thus the present study has demonstrated that nicotinic agonists-induced CA secretion may be associated with a stimulation of uptake and efflux of Ca in bovine adrenal medulla and that nicotinic antagonists may inhibit the stimulated flux of Ca by the action on nicotinic receptors of adrenal chromaffin cells.
