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来自肾上腺髓质儿茶酚胺释放的代谢需求。

The metabolic requirements from catecholamine release from the adrenal medulla.

作者信息

Rubin R P

出版信息

J Physiol. 1969 May;202(1):197-209. doi: 10.1113/jphysiol.1969.sp008804.

Abstract
  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.
摘要
  1. 在急性去神经支配的灌注猫肾上腺上,研究了由乙酰胆碱或钙加高钾引发的儿茶酚胺分泌的代谢需求。

  2. 葡萄糖缺乏加缺氧导致用正常洛克溶液灌注的肾上腺自发儿茶酚胺输出增加,而从灌注培养基中去除钙可消除这种增加。

  3. 缺氧加葡萄糖缺乏并未抑制对低浓度乙酰胆碱重复暴露的分泌反应,但确实抑制了对较高浓度乙酰胆碱的反应。单独或一起施加葡萄糖缺乏和氮气时,均未抑制对钙的总儿茶酚胺输出。对钙诱发分泌的差异分析表明,在缺氧期间,儿茶酚胺输出主要由肾上腺素分泌维持。

  4. 氰化物(0.2 mM)在有葡萄糖存在时增强了对钙的分泌反应,但当从灌注培养基中省略葡萄糖时,氰化物导致钙诱发分泌逐渐下降。碘乙酸(IAA)(0.2 mM)在有氧条件下使对钙的反应降低约50%,在无氧条件下降低90%。

  5. 在缺氧条件下,髓质的糖原含量大幅减少。

  6. 得出的结论是,钙对髓质嗜铬细胞的分泌作用需要能量。能量可能来自糖酵解或氧化代谢。讨论了钙与三磷酸腺苷(ATP)在引发儿茶酚胺分泌中可能的相互作用。

  7. 缺氧期间分泌的肾上腺素和去甲肾上腺素百分比的变化表明,缺氧可能通过外周以及中枢机制调节髓质儿茶酚胺分泌。

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本文引用的文献

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