Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation.
Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation.
复制标题
通过刺激动脉周围神经，血管肾上腺素能神经释放 5-羟色胺诱导血管收缩反应。
DOI：
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发表时间：
1984
影响因子：
3.5
通讯作者：
K. Takasaki
中科院分区：
文献类型：
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作者：
H. Kawasaki;K. Takasaki
在离体大鼠肠系膜血管床灌流模型上，观察了动脉周围神经刺激（PNS）引起血管肾上腺素能神经释放5-羟色胺（5-HT）的缩血管反应。PNS以4 - 16 Hz，2 msec脉冲持续30 sec。用5-HT（1和10 μ M）处理20分钟后，对PNS的升压反应大大增强，对PNS的频率依赖性升压反应再次出现。然而，5-HT治疗并没有改变升压反应输注外源性去甲肾上腺素（0.5和1 nmol）先前降低酚妥拉明。在存在麦角新碱（0.1 μ M）、酮色林（0.1 μ M）、河豚毒素（0.1 μ M）、乙啶（5 μ M）或无Ca++的克雷布斯溶液中，这种增强作用不会发生。此外，在用6-羟基多巴胺处理的制剂中，5-HT处理对消除的PNS反应没有影响。可卡因（10 μ M）或氟西汀（10 μ M），但不能阻止皮质酮（10 μ M）与5-HT一起灌注时的增强。在[~ 3 H]-5-HT预标记的肠系膜血管床中，三七总皂甙引起频率依赖性的氚外排增加，这种增加可被河豚毒素乙啶或6-羟基多巴胺和无Ca ~（++）的Krebs液所阻断。这些结果表明，5-HT在体外被血管肾上腺素能神经末梢摄取，并通过神经刺激释放，导致血管收缩。它也表明，5-HT可能有助于维持局部血管紧张性，通过这种机制在体内。
The vasoconstrictor response to 5-hydroxytryptamine (5-HT) released from vascular adrenergic nerves by periarterial nerve stimulation (PNS) was studied in the perfused mesenteric vascular bed isolated from the rat. PNS was delivered at 4 to 16 Hz, 2 msec in pulse duration for 30 sec. After treatment with 5-HT (1 and 10 microM) for 20 min, the pressor response to PNS, previously decreased by 80 to 90% with phentolamine (0.1 microM), was greatly potentiated and a frequency-dependent pressor response to PNS reappeared. However, the 5-HT treatment did not alter the pressor response to infusion of exogenous norepinephrine (0.5 and 1 nmol) previously decreased by phentolamine. This potentiation did not occur in the presence of methysergide (0.1 microM), ketanserin (0.1 microM), tetrodotoxin (0.1 microM), guanethidine (5 microM) or in Ca++-free Krebs' solution. Also, in the preparation treated with 6-hydroxydopamine, 5-HT treatment had no effect on the abolished PNS response. Either cocaine (10 microM) or fluoxetine (10 microM) but not corticosterone (10 microM) prevented the potentiation when perfused together with 5-HT. In the mesenteric vascular bed prelabeled with [3H]-5-HT, PNS evoked a frequency-dependent increase of tritium efflux, which was abolished by treatment with tetrodotoxin guanethidine or 6-hydroxydopamine and in Ca++-free Krebs' solution. These results suggest that 5-HT is taken up by vascular adrenergic nerve endings in vitro and it is released by nerve stimulation, resulting in vasoconstriction. It is also suggested that 5-HT may contribute to the maintenance of local vascular tone through this mechanism in vivo.