Endothelin-induced modulation of neuropeptide Y and norepinephrine release from the rat mesenteric bed.
Endothelin-induced modulation of neuropeptide Y and norepinephrine release from the rat mesenteric bed.
复制标题
内皮素诱导的神经肽 Y 和去甲肾上腺素从大鼠肠系膜床释放的调节。
DOI：
10.1152/ajpheart.00177.2001
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Westfall,ThomasC
中科院分区：
文献类型：
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作者：
Hoang,Dan;Macarthur,Heather;Gardner,Alice;Westfall,ThomasC
研究了三种内皮素 (ET) 激动剂 [ET-1、ET-3 和沙拉福毒素 (STX6C)] 对神经刺激诱导的大鼠肠系膜动脉床灌注去甲肾上腺素 (NE) 和神经肽 Y 免疫反应性化合物 (NPY-ir) 释放的影响以及对灌注压的影响。 ET-1、ET-3 和 STX6C 均对 NPY-ir 诱发的释放产生显着的、浓度依赖性的降低，但对 NE 的释放没有影响。相比之下，所有三种 ET 均增强了神经刺激引起的灌注压增加。 ET-1 对神经刺激诱导的 NPY-ir 释放的抑制被 ETA/ETB 拮抗剂 PD-142893 和 ETB 拮抗剂 RES-701-1 显着阻断，但不被 ETA 拮抗剂 BQ-123 阻断。 ET-1 对神经刺激引起的灌注压增加的增强作用被 PD-142893 和 BQ-123 显着阻断，并被 RES-701-1 减弱。预先将制剂暴露于吲哚美辛或甲氯芬那酯未能改变NPY-ir诱发释放的减弱或ET-1或ET-3产生的灌注压增加的增强。这些结果与交感神经递质可以优先由血管神经效应器连接处的旁分泌介质调节的观点一致。
The effect of three endothelin (ET) agonists [ET-1, ET-3, and sarafotoxin (STX6C)] on the nerve stimulation-induced release of norepinephrine (NE) and neuropeptide Y-immunoreactive compounds (NPY-ir) from the perfused mesenteric arterial bed of the rat as well as the effect on perfusion pressure were examined. ET-1, ET-3, and STX6C all produced a significant, concentration-dependent decrease in the evoked release of NPY-ir but had no effect on the release of NE. In contrast, all three ETs potentiated the nerve stimulation-induced increase in perfusion pressure. The inhibition of nerve stimulation-induced NPY-ir release by ET-1 was significantly blocked by the ETA/ETBantagonist PD-142893 and the ETBantagonist RES-701-1 but not by the ETAantagonist BQ-123. The potentiation of the nerve stimulation-induced increase in perfusion pressure by ET-1 was significantly blocked by PD-142893 and BQ-123 and attenuated by RES-701-1. Prior exposure of the preparation to indomethacin or meclofenamate failed to alter the attenuation of the evoked release of NPY-ir or the potentiation of the increase in perfusion pressure produced by ET-1 or ET-3. These results are consistent with the idea that sympathetic cotransmitters can be preferentially modulated by paracrine mediators at the vascular neuroeffector junction.