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氯化钾诱发猫交感神经去甲肾上腺素外流:双重作用机制。

Norepinephrine efflux evoked by potassium chloride in cat sympathetic nerves: dual mechanism of action.

作者信息

Yamazaki T, Akiyama T, Kawada T, Kitagawa H, Takauchi Y, Yahagi N, Sunagawa K

机构信息

Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565, Japan.

出版信息

Brain Res. 1998 May 25;794(1):146-50. doi: 10.1016/s0006-8993(98)00209-1.

Abstract

Using a dialysis technique, prominent efflux of norepinephrine (NE) from cardiac sympathetic nerve endings was observed under local administration of potassium chloride (KCl, 100 mM). KCl induced NE efflux was suppressed by omega-conotoxin GVIA or desipramine but residual efflux of NE was still detectable. In the presence of omega-conotoxin GVIA, KCl induced efflux of NE was augmented by pretreatment with reserpine, indicating that this efflux of NE was derived from axoplasma with neurotransporter. These data suggest that a KCl induced brisk increase in dialysate NE levels might occur as a consequence of exocytotic NE release and carrier mediated outward NE transport from nerve endings.

摘要

采用透析技术,在局部给予氯化钾(KCl,100 mM)的情况下,观察到心脏交感神经末梢有显著的去甲肾上腺素(NE)流出。ω-芋螺毒素GVIA或地昔帕明可抑制KCl诱导的NE流出,但仍可检测到NE的残余流出。在存在ω-芋螺毒素GVIA的情况下,利血平预处理可增强KCl诱导的NE流出,表明这种NE流出源自含有神经递质转运体的轴浆。这些数据表明,KCl诱导的透析液NE水平迅速升高可能是由于NE通过胞吐作用释放以及载体介导的NE从神经末梢向外转运所致。

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