Frye R A, Holz R W
J Neurochem. 1984 Jul;43(1):146-50. doi: 10.1111/j.1471-4159.1984.tb06690.x.
Increased arachidonic acid release occurred during activation of catecholamine secretion from cultured bovine adrenal medullary chromaffin cells. The nicotinic agonist 1,1-dimethyl-4- phenylpiperazinium (DMPP) caused an increased release of preincubated [3H]arachidonic acid over a time course which corresponded to the stimulation of catecholamine secretion. Like catecholamine secretion, the DMPP-induced [3H]arachidonic acid release was calcium-dependent and was blocked by the nicotinic antagonist mecamylamine. Depolarization by elevated K+, which induced catecholamine secretion, also stimulated arachidonic acid release. Because arachidonic acid release from cells probably results from phospholipase A2 activity, our findings indicate that phospholipase A2 may be activated in chromaffin cells during secretion.
培养的牛肾上腺髓质嗜铬细胞在儿茶酚胺分泌激活过程中，花生四烯酸释放增加。烟碱激动剂1,1 - 二甲基 - 4 - 苯基哌嗪鎓（DMPP）在与儿茶酚胺分泌刺激相对应的时间进程中，引起预孵育的[3H]花生四烯酸释放增加。与儿茶酚胺分泌一样，DMPP诱导的[3H]花生四烯酸释放依赖于钙，并被烟碱拮抗剂美加明阻断。升高钾离子引起的去极化诱导儿茶酚胺分泌，同时也刺激花生四烯酸释放。由于细胞中花生四烯酸的释放可能源于磷脂酶A2的活性，我们的研究结果表明，在分泌过程中嗜铬细胞中的磷脂酶A2可能被激活。
