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The metabolic requirements for catecholamine release from the adrenal medulla

机译:儿茶酚胺从肾上腺髓质释放的代谢要求

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摘要

1. The metabolic requirements for catecholamine secretion elicited by acetylcholine or by calcium plus high K+ were studied on acutely denervated perfused cat adrenal glands.2. Glucose-deprivation plus anoxia caused an increase in the spontaneous catecholamine output from adrenal glands perfused with normal Locke solution, which was abolished by the removal of calcium from the perfusion medium.3. Anoxia plus glucose-deprivation did not depress the secretory response to repeated exposures of a low concentration of acetylcholine, but did depress the response to a higher concentration of acetylcholine. Glucose-deprivation and nitrogen, when imposed either separately or together, did not inhibit total catecholamine output in response to calcium. Differential analysis of the calcium-evoked secretion showed that during anoxia, catecholamine output was maintained primarily by adrenaline secretion.4. Cyanide (0·2 mM) potentiated the secretory response to calcium in the presence of glucose, but when glucose was omitted from the perfusion medium, cyanide caused a gradual decline in calcium-evoked secretion. Iodoacetic acid (IAA) (0·2 mM) depressed the response to calcium by about 50% under aerobic conditions and by 90% under anaerobic conditions.5. The glycogen content of medullae was profoundly depleted under anoxic conditions.6. It is concluded that energy is required for the secretory action of calcium on medullary chromaffin cells. The energy may be derived from glycolysis or oxidative metabolism. A possible interaction between calcium and adenosine triphosphate acid (ATP) in eliciting catecholamine secretion is discussed.7. The alteration in the percent adrenaline and noradrenaline secreted during anoxia indicates that anoxia may regulate medullary catecholamine secretion through a peripheral, as well as a central mechanism.
机译:1.研究了急性失神经的灌注猫肾上腺由乙酰胆碱或钙加高K + 引起的儿茶酚胺分泌的代谢需求。2。缺糖加缺氧导致正常洛克溶液灌输的肾上腺自发儿茶酚胺产量增加,其通过从灌注介质中去除钙而被消除。3。缺氧加葡萄糖剥夺没有抑制对低浓度乙酰胆碱反复暴露的分泌反应,但确实抑制了对较高浓度乙酰胆碱的反应。当单独或一起使用葡萄糖剥夺和氮时,它们不会抑制钙对儿茶酚胺的总输出。钙诱发的分泌物的差异分析表明,在缺氧期间,儿茶酚胺的输出主要是由肾上腺素分泌维持的。4。在存在葡萄糖的情况下,氰化物(0·2 mM)增强了对钙的分泌反应,但是当灌注介质中缺少葡萄糖时,氰化物导致钙诱发的分泌逐渐减少。碘乙酸(IAA)(0·2 mM)在有氧条件下使对钙的响应降低了约50%,在无氧条件下降低了90%。5。在缺氧条件下,延髓的糖原含量明显减少。6。结论是,钙对髓质嗜铬细胞的分泌作用需要能量。能量可以来自糖酵解或氧化代谢。讨论了钙和三磷酸腺苷(ATP)之间可能的相互作用,引起儿茶酚胺分泌。7。缺氧过程中分泌的肾上腺素和去甲肾上腺素百分比的变化表明,缺氧可能通过周围以及中央机制调节髓质儿茶酚胺的分泌。

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