Co-release and functional interactions of neuropeptide Y and noradrenaline in peripheral sympathetic vascular control.
Co-release and functional interactions of neuropeptide Y and noradrenaline in peripheral sympathetic vascular control.
复制标题
神经肽 Y 和去甲肾上腺素在外周交感血管控制中的共同释放和功能相互作用。
DOI：
--
复制
发表时间：
1988
期刊：
影响因子：
--
通讯作者：
J. Pernow
中科院分区：
文献类型：
--
作者：
J. Pernow
1.免疫组化结果表明，NPY-LI与NA共存于骨骼肌交感动脉周围神经中。相应的静脉与很少或没有交感神经相关联。2. SNS诱发了一个可检测的溢出从狗股薄肌在体内在高频，但不是低频刺激。α-肾上腺素能受体拮抗剂给药后，NPY-LI的溢出增强，表明通过类似于NA的机制的连接前抑制释放。利血平预处理可使骨骼肌NA和NPY-LI减少。利血平诱导的NPY-LI，但不是NA的消耗，是高度依赖于完整的神经活动，因为它是防止分散。3.缓慢发展和持久的血管收缩引起的外源性神经肽Y和高频率的SNS在股薄肌中的肾上腺素能受体拮抗剂的存在下，完全阻断了血管收缩反应的外源性NA。利血平处理后，相当大的血管收缩反应，SNS观察到在分散的肌肉比完整的，在平行的溢出的NPY-LI。这些结果表明，释放的神经肽Y可能是介导的肾上腺素受体拮抗剂和利血平抵抗的功能反应，SNS在股薄肌。ATP机制似乎是不太重要的交感神经控制股薄肌血管。4.运动时血浆NPY-LI和NA水平升高，提示交感神经共同释放。由于酚妥拉明和可乐定分别增强和抑制运动诱导的血浆NPY-LI和NA水平的增加，这种释放似乎被α-肾上腺素能受体的激活所衰减。血浆中的NPY-LI水平增加，在控制条件下，可乐定和酚妥拉明改变，主要是在高工作负荷，这可能表明优先释放的肽在高水平的交感神经活性。5.当地内务部在低nmolar范围内的血浆浓度下，人的NPY输注降低了前臂血流量，具有阈值效应。NPY引起的前臂血流量减少比NA引起的持续时间长得多，这可能部分与NPY的代谢半衰期长有关。6. NPY在体外诱导的收缩效应在不同的动脉和静脉之间变化。最明显的效果是诱发在小的人骨骼肌动脉，其中NPY引起的最大收缩相似的NA。（400字处截断摘要）
1. The immunohistochemical results suggest that NPY-LI co-exists with NA in sympathetic periarterial nerves of skeletal muscle. The corresponding veins are associated with few or no sympathetic nerves. 2. SNS evoked a detectable overflow of NPY-LI from the dog gracilis muscle in vivo during high-frequency but not low-frequency stimulation. After the administration of alpha-adrenoceptor antagonists, the overflow of NPY-LI was enhanced, indicating prejunctional inhibition of release via a mechanism similar to that for NA. Reserpine pretreatment depleted both NA and NPY-LI from skeletal muscle. The reserpine-induced depletion of NPY-LI, but not of NA, was highly dependent on intact nerve activity, since it was prevented by decentralization. 3. Slowly developing and long-lasting vasoconstriction was evoked by exogenous NPY and by high-frequency SNS in the gracilis muscle in the presence of adrenoceptor antagonists that completely blocked the vasoconstrictor response to exogenous NA. After reserpine treatment, considerably larger vasoconstrictor responses to SNS were observed in the decentralized muscle than in the intact one, in parallel with the overflow of NPY-LI. These results suggest that the released NPY may be the mediator of the adrenoceptor antagonist- and reserpine-resistant functional responses to SNS in the gracilis muscle. ATP mechanisms seem to be of less importance for the sympathetic control of gracilis muscle vasculature. 4. The plasma levels of NPY-LI and NA in man increased during physical exercise, suggesting a co-release from sympathetic nerves. This release appears to be attenuated by activation of alpha-adrenoceptors since phentolamine and clonidine, respectively, enhanced and suppressed the exercise-induced increase in the plasma levels of both NPY-LI and NA. The plasma levels of NPY-LI were increased during control conditions, and altered by clonidine and phentolamine, mainly at high work loads, which may indicate preferential release of the peptide at high levels of sympathetic activity. 5. Local i.a. infusion of NPY in man reduced forearm blood flow with a threshold effect at a plasma concentration in the low nmolar range. The reduction in forearm blood flow induced by NPY was considerably more long-lasting than that evoked by NA, which may partly be related to the long metabolic half-life of NPY. 6. NPY induced contractile effects in vitro that varied between different arteries and veins. The most pronounced effects were evoked in small human skeletal muscle arteries, where NPY caused a maximal contraction similar to that of NA.(ABSTRACT TRUNCATED AT 400 WORDS)