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花生四烯酸代谢抑制剂对培养的肾上腺嗜铬细胞钙摄取和儿茶酚胺释放的影响。

Effects of inhibitors of arachidonic acid metabolism on calcium uptake and catecholamine release in cultured adrenal chromaffin cells.

作者信息

Sasakawa N, Yamamoto S, Kato R

出版信息

Biochem Pharmacol. 1984 Sep 1;33(17):2733-8. doi: 10.1016/0006-2952(84)90689-0.

Abstract

The possibility that arachidonic acid metabolism is involved in the secretory process in cultured adrenal chromaffin cells was investigated by studying the effects of lipoxygenase inhibitors and cyclooxygenase inhibitors on 45Ca2+ uptake and catecholamine release. Lipoxygenase inhibitors, which have different chemical structures, such as nordihydroguaiaretic acid (NDGA), 3-amino-1-(3-trifluoromethylphenyl)-2-pyrazoline (BW755C) and 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA861) all prevented the catecholamine release evoked by carbamylcholine and high K+. In contrast, cyclooxygenase inhibitors, such as aspirin and indomethacin failed to inhibit the carbamylcholine-evoked catecholamine release. Lipoxygenase inhibitors also inhibited 45Ca2+ uptake into the cells stimulated by carbamylcholine and high K+. Lipoxygenase inhibitors inhibited 45Ca2+ uptake and catecholamine release with similar potency. Slightly higher concentrations of lipoxygenase inhibitors were required to inhibit high K+-evoked effects compared to those evoked by carbamylcholine. The inhibitory effects of these inhibitors on carbamylcholine-evoked catecholamine release was different in its nature from the inhibitory effect of verapamil, a blocker of the Ca2+ channel, and was not due to a competitive antagonism at cholinergic receptor site. Moreover, these lipoxygenase inhibitors did not inhibit the binding of [3H]nitrendipine to chromaffin cell homogenate. The data suggest that lipoxygenase inhibitors prevent the catecholamine release from cultured adrenal chromaffin cells by blocking Ca2+ uptake. It might be possible that lipoxygenase product(s) is involved in the Ca2+ translocation system in these cells.

摘要

通过研究脂氧合酶抑制剂和环氧化酶抑制剂对45Ca2+摄取及儿茶酚胺释放的影响,探讨了花生四烯酸代谢参与培养的肾上腺嗜铬细胞分泌过程的可能性。具有不同化学结构的脂氧合酶抑制剂,如去甲二氢愈创木酸(NDGA)、3-氨基-1-(3-三氟甲基苯基)-2-吡唑啉(BW755C)和2,3,5-三甲基-6-(12-羟基-5,10-十二碳二炔基)-1,4-苯醌(AA861),均能阻止氨甲酰胆碱和高钾诱发的儿茶酚胺释放。相比之下,环氧化酶抑制剂,如阿司匹林和吲哚美辛,未能抑制氨甲酰胆碱诱发的儿茶酚胺释放。脂氧合酶抑制剂还抑制了氨甲酰胆碱和高钾刺激的细胞对45Ca2+的摄取。脂氧合酶抑制剂抑制45Ca2+摄取和儿茶酚胺释放的效力相似。与氨甲酰胆碱诱发的效应相比,抑制高钾诱发的效应需要略高浓度的脂氧合酶抑制剂。这些抑制剂对氨甲酰胆碱诱发的儿茶酚胺释放的抑制作用在性质上不同于Ca2+通道阻滞剂维拉帕米的抑制作用,且不是由于在胆碱能受体部位的竞争性拮抗作用。此外,这些脂氧合酶抑制剂不抑制[3H]尼群地平与嗜铬细胞匀浆的结合。数据表明,脂氧合酶抑制剂通过阻断Ca2+摄取来阻止培养的肾上腺嗜铬细胞释放儿茶酚胺。脂氧合酶产物可能参与了这些细胞中的Ca2+转运系统。

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