...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Norepinephrine induced alpha-adrenoceptor mediated increase in rat brain Na-K ATPase activity is dependent on calcium ion.
【24h】

Norepinephrine induced alpha-adrenoceptor mediated increase in rat brain Na-K ATPase activity is dependent on calcium ion.

机译：去甲肾上腺素诱导的α-肾上腺素能受体介导的大鼠脑Na-K ATPase活性增加取决于钙离子。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

It has been reported that norepinephrine increases Na-K ATPase activity by acting on alpha-1 adrenoceptors. The mechanism of such an increase was investigated. The norepinephrine induced increase in synaptosomal Na-K ATPase activity was prevented by pretreating the rat brain homogenate with either EDTA, a divalent cation chelator or prazosin, an alpha-1 adrenoceptor blocker. The norepinephrine and EGTA increased the Na-K ATPase activity in the synaptosome prepared from rat brain homogenate untreated with EDTA. The EGTA was ineffective in stimulating the enzyme activity if the synaptosome was prepared from homogenate treated with norepinephrine. However, the EGTA was effective in increasing the enzyme activity if the synaptosome was prepared from the homogenate treated with norepinephrine in the presence of prazosin. Thus, norepinephrine did not increase the Na-K ATPase activity in the presence of EDTA or alpha-1 adrenoceptor blocker. Similarly, the Ca++ chelator, EGTA, could not increase the enzyme activity if the homogenate was pretreated with norepinephrine alone. However, if norepinephrine action was blocked by alpha-1 antagonist prazosin, EGTA increased the enzyme activity possibly by chelation of Ca++. Further, chlorotetracycline fluorescence study showed that norepinephrine removes membrane bound Ca++. Thus, it is likely that norepinephrine acts on adrenoceptors and removes membrane bound Ca++ and thereby increases the Na-K ATPase activity in the synaptosome.
机译：据报道，去甲肾上腺素通过作用于α-1肾上腺素受体而增加Na-K ATPase活性。研究了这种增加的机理。通过用二价阳离子螯合剂EDTA或α-1肾上腺素受体阻滞剂prazosin对大鼠脑匀浆进行预处理，可以防止去甲肾上腺素诱导的突触体Na-K ATPase活性增加。去甲肾上腺素和EGTA可增加由未经EDTA处理的大鼠脑匀浆制备的突触体中的Na-K ATPase活性。如果用去甲肾上腺素处理过的匀浆制备突触体，EGTA不能有效地刺激酶的活性。但是，如果在哌唑嗪存在下由去甲肾上腺素处理过的匀浆制备突触小体，EGTA可有效提高酶的活性。因此，在EDTA或α-1肾上腺素受体阻滞剂存在下，去甲肾上腺素不会增加Na-K ATPase活性。同样，如果仅用去甲肾上腺素预处理匀浆，则Ca ++螯合剂EGTA不会增加酶的活性。但是，如果去甲肾上腺素的作用被α-1拮抗剂哌唑嗪阻断，则EGTA可能通过螯合Ca ++来增加酶的活性。此外，氯四环素荧光研究表明，去甲肾上腺素可去除膜结合的Ca ++。因此，去甲肾上腺素可能作用于肾上腺素受体并去除膜结合的Ca ++，从而增加突触体中的Na-K ATPase活性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号