Arachidonic acid regulation of vasopressin release and intracellular Ca2+ in neurohypophysial nerve endings.
Arachidonic acid regulation of vasopressin release and intracellular Ca2+ in neurohypophysial nerve endings.
复制标题
花生四烯酸对神经垂体神经末梢加压素释放和细胞内 Ca2+ 的调节。
DOI：
10.1016/s0006-8993(96)00973-0
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发表时间：
1996
期刊：
影响因子：
2.9
通讯作者：
Nordmann,JJ
中科院分区：
文献类型：
--
作者：
Stuenkel,EL;Dayanithi,G;Nordmann,JJ
本文研究了花生四烯酸（AA）及其代谢产物对大鼠神经垂体完整神经末梢和链溶素-O（streptolysin-O）透化神经末梢加压素分泌和细胞内游离钙浓度（[Ca ~（2+）]i）的影响。花生四烯酸诱导完整和链球菌溶血素-O透化的神经末梢中静息加压素（AVP）分泌呈剂量依赖性增加。虽然AA也剂量依赖性地诱导完整神经末梢[Ca 2 +] i的增加，但AA诱导的分泌反应在很大程度上不依赖于[Ca 2 +]i的增加。在完整的神经末梢的分泌反应表明AA诱导的分泌是持续的，AA诱导的加压素分泌发生通过胞吐。花生四烯酸也剂量依赖性地增强K+去极化诱发的加压素释放。尽管AA诱导的K+诱发的Ca 2+内流减少，但分泌增强。此外，AA重新启动分泌后，在Ca 2+依赖的胞吐分泌反应的下降，这表明一个单独的分泌机制，从Ca 2+诱导的分泌。AA代谢途径的抑制表明AA本身介导分泌作用，AA可能通过脂氧合酶快速代谢。
The effects of arachidonic acid (AA) and arachidonic acid metabolites on vasopressin secretion and on intracellular free calcium concentration ([Ca2+]i) from both intact and streptolysin-O permeabilized isolated nerve endings of the rat neurohypophysis were studied. Arachidonic acid induced a dose-dependent increase in resting vasopressin (AVP) secretion in both intact and streptolysin-O permeabilized nerve endings. Although AA also dose-dependently induced an increase in [Ca2+]iin intact nerve endings, the AA-induced secretory response was largely independent of an increase in [Ca2+]i. Secretory responses in intact nerve endings showed AA-induced secretion to be sustained and that AA-induced vasopressin secretion occurs via exocytosis. Arachidonic acid also dose-dependently potentiated K+-depolarization evoked vasopressin release. The potentiation of secretion occurred despite an AA-induced reduction in K+-evoked Ca2+influx. In addition, AA reinitiated secretion following a decline in the Ca2+-dependent exocytotic secretory response suggesting a separate secretory mechanism from Ca2+-induced secretion. Inhibition of the metabolic pathways for AA suggested that AA itself mediates the secretory effects and that AA is likely subject to rapid metabolism by lipoxygenases.