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Effects of ouabain on in situ cardiac sympathetic nerve endings.

机译:哇巴因对原位心脏交感神经末梢的影响。

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Using dialysis technique, the effects of ouabain on in situ cardiac sympathetic nerve endings were examined in anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and the concentration of dialysate norepinephrine (NE) was used as an indicator of NE output at the cardiac sympathetic nerve ending. Locally applied ouabain dose-dependently (1, 10, 100 microM) increased dialysate NE levels. This finding suggested that ouabain causes an increase in NE efflux without any requirement for prior mobilization of NE from vesicular stores. Transection of sympathetic nerves innervating the heart, was without effect on the ouabain (100 microM)-induced increase in NE efflux. Pretreatment with a Ca2+-channel blocker, omega-conotoxin GVIA (10 microg/kg i.v.) suppressed the ouabain-induced NE efflux. These data suggested that ouabain opened N-type calcium channels coupled to NE release without centrally mediated neural transmission. Furthermore, ouabain-induced NE efflux was suppressed by pretreatment with desipramine (neuronal NE uptake inhibitor, 100 microM). Our data suggest that the two mechanisms (exocytosis and carrier-mediated outward transport), to the same extent, contributed to the amount of NE efflux evoked by ouabain in in situ cardiac sympathetic nerve endings.
机译:使用透析技术,在麻醉的猫中检查了哇巴因对原位心脏交感神经末梢的影响。将透析探针植入左心室心肌,并将透析液去甲肾上腺素(NE)的浓度用作心脏交感神经末梢NE输出的指标。局部应用哇巴因剂量依赖性(1、10、100 microM)增加了透析液NE水平。该发现表明,哇巴因引起NE外排的增加,而无需事先从囊泡贮藏中动员NE。交感神经支配心脏,对哇巴因(100 microM)引起的NE外排增加没有影响。用Ca2 +通道阻滞剂预处理,ω-芋螺毒素GVIA(10 microg / kg静脉内)抑制了哇巴因诱导的NE外排。这些数据表明,哇巴因打开了N型钙通道,与NE释放耦合而没有中枢介导的神经传递。此外,哇巴因诱导的NE外排通过用地昔帕明(神经元NE摄取抑制剂,100 microM)预处理而被抑制。我们的数据表明,这两种机制(胞吐作用和载体介导的向外转运)在相同程度上促进了哇巴因在原位心脏交感神经末梢引起的NE外排量。

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