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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 >Reverse Na(+)/Ca(2+)-exchange mediated Ca(2+)-entry and noradrenaline release in Na(+)-loaded peripheral sympathetic nerves.
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Reverse Na(+)/Ca(2+)-exchange mediated Ca(2+)-entry and noradrenaline release in Na(+)-loaded peripheral sympathetic nerves.

机译：反向Na（+）/ Ca（2+）交换介导的Ca（2+）条目和去甲肾上腺素释放在Na（+）加载的周围交感神经中。

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摘要

[(3)H]noradrenaline ([(3)H]NA) released from sympathetic nerves in the isolated main pulmonary artery of the rabbit was measured in response to field stimulation (2Hz, 1ms, 60V for 3min) in the presence of uptake blockers (cocaine, 3 x10(-5)M and corticosterone, 5 x10(-5)M). The [(3)H]NA-release was fully blocked by the combined application of the selective and irreversible 'N-type' voltage-sensitive Ca(2+)-channel (VSCC)-blocker omega-conotoxin (omega-CgTx) GVIA (10(-8)M) and the 'non-selective' VSCC-blocker aminoglycoside antibiotic neomycin (3x10(-3)M). Na(+)-loading (Na(+)-pump inhibition by K(+)-free perfusion) was required to elicit further NA-release after blockade of VSCCs (omega-CgTx GVIA+neomycin). In K(+)-free solution, in the absence of functioning VSCCs (omega-CgTx GVIA+neomycin), the fast Na(+)-channel activator veratridine (10(-5)M) further potentiated the nerve-evoked release of [(3)H]NA. This NA-release was significantly inhibited by KB-R7943, and fully blocked by Ca(o)(2+)-removal. However, Li(+)-substitution was surprisingly ineffective. The non-selective K(+)-channel blocker 4-aminopyridine (4-AP, 10(-4)M) also further potentiated the nerve-evoked release of NA in K(+)-free solution. This potentiated release was concentration-dependently inhibited by KB-R7943, significantly inhibited by Li(+)-substitution and abolished by Ca(o)(2+)-removal. It is concluded that in Na(+)-loaded sympathetic nerves, in which the VSCCs are blocked, the reverse Na(+)/Ca(2+)-exchange-mediated Ca(2+)-entry is responsible for transmitter release on nerve-stimulation. Theoretically we suppose that the fast Na(+)-channel and the exchanger proteins are close to the vesicle docking sites.
机译：在有摄取的情况下，响应野外刺激（2Hz，1ms，60V 3min），测量从离体兔主肺动脉交感神经中释放的[（3）H]去甲肾上腺素（[（3）H] NA）阻断剂（可卡因3 x10（-5）M和皮质酮5 x10（-5）M）。 [（3）H] NA释放被选择性和不可逆的'N型'电压敏感Ca（2+）通道（VSCC）受体阻滞剂ω-芋螺毒素（omega-CgTx）的组合应用完全阻止GVIA（10（-8）M）和“非选择性” VSCC阻断剂氨基糖苷抗生素新霉素（3x10（-3）M）。需要Na（+）-加载（Na（+）-泵抑制通过无K（+）的灌注）来引发VSCCs（Ω-CgTxGVIA +新霉素）阻断后进一步的NA释放。在无K（+）的溶液中，在没有功能性VSCC（omega-CgTx GVIA +新霉素）的情况下，快速的Na（+）通道激活剂veratridine（10（-5）M）进一步增强了神经诱发的释放[（3）H] NA。此NA释放被KB-R7943显着抑制，并被Ca（o）（2+）去除完全阻止。但是，Li（+）替代出奇地无效。非选择性K（+）通道阻滞剂4-氨基吡啶（4-AP，10（-4）M）还进一步增强了神经诱发的NA在无K（+）溶液中的释放。此增强的释放受到KB-R7943的浓度依赖性抑制，被Li（+）取代显着抑制，而被Ca（o）（2+）去除则被消除。结论是，在加载了Na（+）的交感神经中，VSCC受阻，反向的Na（+）/ Ca（2 +）-交换介导的Ca（2+）条目负责释放递质。神经刺激。从理论上讲，我们假设快速Na（+）通道和交换蛋白接近囊泡停靠位点。

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