肾上腺髓质细胞原代培养物对22Na+的摄取及儿茶酚胺分泌

22Na+ uptake and catecholamine secretion by primary cultures of adrenal medulla cells.

作者信息

Amy C, Kirshner N

出版信息

J Neurochem. 1982 Jul;39(1):132-42. doi: 10.1111/j.1471-4159.1982.tb04711.x.

DOI:10.1111/j.1471-4159.1982.tb04711.x

Abstract

The uptake of 22Na+ and secretion of catecholamines by primary cultures of adrenal medulla cells under the influence of a variety of agonists and antagonists were determined. Veratridine, batrachotoxin, scorpion venom, and nicotine caused a parallel increase in 22Na+ uptake and Ca2+-dependent catecholamine secretion. Ba2+, depolarizing concentrations of K+, and the Ca2+ ionophore Ionomycin stimulated secretion of catecholamines but did not increase the uptake of 22Na+. Tetrodotoxin inhibited both 22Na+ uptake and catecholamine secretion evoked by veratridine, batrachotoxin, and scorpion venom, but had no effect on 22Na+ uptake and catecholamine secretion caused by nicotine. On the other hand, histrionicotoxin, which blocks the acetylcholine receptor-linked ion conductance channel, blocked nicotine-stimulated 22Na+ uptake and catecholamine secretion, but only partially inhibited veratridine-stimulated catecholamine secretion and had no effect on veratridine-stimulated 22Na+ uptake. The combination of veratridine plus tetrodotoxin, which has been shown to prevent nicotine-stimulated secretion of catecholamines by adrenal medulla cells, also prevented nicotine-stimulated 22Na+ uptake by the primary cultures. These studies demonstrate the presence of tetrodotoxin-sensitive Na+ channels in adrenal medulla cells which are functionally linked to Ca2+-dependent catecholamine secretion. However, These channels are not utilized for Na+ entry upon activation of nicotinic receptors; in this case Na+ entry occurs through the receptor-associated ion conductance channel.

摘要

测定了在多种激动剂和拮抗剂影响下肾上腺髓质细胞原代培养物对(^{22}Na^+)的摄取及儿茶酚胺的分泌情况。藜芦碱、蛙毒素、蝎毒和尼古丁可使(^{22}Na^+)摄取及(Ca^{2 +})依赖性儿茶酚胺分泌同时增加。(Ba^{2 +})、去极化浓度的(K^+)以及(Ca^{2 +})离子载体离子霉素可刺激儿茶酚胺分泌，但不增加(^{22}Na^+)摄取。河豚毒素可抑制藜芦碱、蛙毒素和蝎毒诱发的(^{22}Na^+)摄取及儿茶酚胺分泌，但对尼古丁引起的(^{22}Na^+)摄取及儿茶酚胺分泌无影响。另一方面，阻断乙酰胆碱受体相关离子电导通道的组氨酸毒素可阻断尼古丁刺激的(^{22}Na^+)摄取及儿茶酚胺分泌，但仅部分抑制藜芦碱刺激的儿茶酚胺分泌，对藜芦碱刺激的(^{22}Na^+)摄取无影响。已证明藜芦碱加河豚毒素可阻止肾上腺髓质细胞尼古丁刺激的儿茶酚胺分泌，同时也可阻止原代培养物中尼古丁刺激的(^{22}Na^+)摄取。这些研究表明，肾上腺髓质细胞中存在对河豚毒素敏感的(Na^+)通道，其在功能上与(Ca^{2 +})依赖性儿茶酚胺分泌相关联。然而，这些通道在烟碱受体激活时不用于(Na^+)内流；在这种情况下，(Na^+)内流通过受体相关离子电导通道发生。