Pinto J E
Horm Metab Res. 1979 Jun;11(6):404-7. doi: 10.1055/s-0028-1092749.
The blocking action of Mg++ on catecholamine release induced by the substitution of extracellular Na+ by an osmotic equivalent amount of sucrose was studied in isolated, perfused bovine adrenal glands. Perfusing glands with 10 mM Mg++ produced at 51.1% inhibition on catecholamine release evoked by Na+ omission. Increasing the concentration of Mg++ to 20 mM this inhibitory effect was enhanced to 90.3%. D-600 (0.3 mM) promoted a marked blockade of acetylcholine-induced release of catechol hormones that was partially and significantly reverted increasing the concentration of Ca++ in the perfusion medium. D-600 (0.3 mM) failed to inhibit the catecholamine-releasing effect of Na+ deprivation. In adrenal glands previously perfused with D-600 (0.3 mM) and then exposed to a Locke solution containing D-600 (0.3 mM) + Mg++ (10 or 20 mM) the inhibition of the secretory responses evoked by the omission of Na+ was of the same magnitude as that obtained when the glands were perfused with Mg++ (10 or 20 mM) in the absence of D-600. These results are compatible with the view that the blocking effect of Mg++ may involve an intracellular site of action and that the access of Mg++ into the chromaffin cell may not be mediated through the Ca++ channels.
在离体灌注的牛肾上腺中，研究了Mg++对用等渗量蔗糖替代细胞外Na+所诱导的儿茶酚胺释放的阻断作用。用10 mM Mg++灌注腺体，对因Na+缺失引起的儿茶酚胺释放产生了51.1%的抑制作用。将Mg++浓度增加到20 mM，这种抑制作用增强到90.3%。D - 600（0.3 mM）显著阻断了乙酰胆碱诱导的儿茶酚胺激素释放，通过增加灌注培养基中Ca++的浓度，这种阻断作用部分且显著地得到逆转。D - 600（0.3 mM）未能抑制Na+缺失引起的儿茶酚胺释放效应。在预先用D - 600（0.3 mM）灌注然后暴露于含有D - 600（0.3 mM）+ Mg++（10或20 mM）的洛克溶液中的肾上腺中，因Na+缺失引起的分泌反应的抑制程度与在没有D - 600的情况下用Mg++（10或20 mM）灌注腺体时获得的抑制程度相同。这些结果与以下观点一致，即Mg++的阻断作用可能涉及细胞内作用位点，并且Mg++进入嗜铬细胞可能不是通过Ca++通道介导的。
