Donoso M V, Brown N, Carrasco C, Cortes V, Fournier A, Huidobro-Toro J P
Departamento de Fisiología, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago.
J Neurochem. 1997 Sep;69(3):1048-59. doi: 10.1046/j.1471-4159.1997.69031048.x.
Neuropeptide Y (NPY) appears to be involved in the sympathetic regulation of vascular tone. To assess the putative role of NPY in mesenteric circulation, the release and biological effect of NPY were examined after electrical stimulation of perimesenteric arterial nerves. Nerve stimulation with trains of 2-30 Hz increased the perfusion pressure of the arterially perfused rat mesenteric bed in a frequency- and time-dependent fashion. Trains of 15-30 Hz significantly displaced to the left, approximately threefold, the noradrenaline (NA)-induced pressor concentration-response curve, in addition to increasing significantly its efficacy. Perfusion with 10 nM exogenous NPY mimicked the electrical stimulation effect, causing a threefold leftward shift of the NA concentration-response curve and increasing the maximal NA response. These effects were antagonized by 100 nM BIBP 3226, indicating the activity of NPY-Y1 receptors. Electrical stimulation of the perimesenteric nerves released immunoreactive NPY (ir-NPY) in a frequency-dependent fashion; the ir-NPY coelutes with synthetic NPY as confirmed by HPLC. Both the electrically induced pressor response and the calcium-dependent release of NPY were obliterated in preparations perfused with 1 microM guanethidine or in rats pretreated intravenously for 48 h with 6-hydroxydopamine, thus revealing the sympathetic origin of these phenomena. Only a small proportion of the total NPY content in the perimesenteric arterial nerves is released after electrical stimulation. Chromatographic studies of the physiological sources of the ir-NPY support that NPY fragments are generated via peptidase degradation. The present findings demonstrate that NPY is released from the perimesenteric arterial sympathetic nerves and acts, via the activation of NPY-Y1 receptors, as the mediator responsible for the potentiation of NA's effect on perfusion pressure in the isolated rat mesenteric bed.
神经肽Y（NPY）似乎参与了血管张力的交感神经调节。为了评估NPY在肠系膜循环中的假定作用，在电刺激肠系膜周围动脉神经后，检测了NPY的释放及其生物学效应。以2 - 30Hz的串刺激神经，以频率和时间依赖性方式增加了动脉灌注大鼠肠系膜床的灌注压力。除了显著提高其效力外，15 - 30Hz的串刺激使去甲肾上腺素（NA）诱导的升压浓度 - 反应曲线向左显著移位约三倍。用10nM外源性NPY灌注模拟了电刺激效应，使NA浓度 - 反应曲线向左移位三倍，并增加了NA的最大反应。这些效应被100nM BIBP 3226拮抗，表明NPY - Y1受体的活性。电刺激肠系膜周围神经以频率依赖性方式释放免疫反应性NPY（ir - NPY）；如通过高效液相色谱法所证实的，ir - NPY与合成NPY共洗脱。在用1μM胍乙啶灌注的制剂中或在静脉内用6 - 羟基多巴胺预处理48小时的大鼠中，电诱导的升压反应和NPY的钙依赖性释放均被消除，从而揭示了这些现象的交感神经起源。电刺激后，肠系膜周围动脉神经中总NPY含量只有一小部分被释放。对ir - NPY生理来源的色谱研究支持NPY片段是通过肽酶降解产生的。目前的研究结果表明，NPY从肠系膜周围动脉交感神经释放，并通过激活NPY - Y1受体，作为负责增强NA对离体大鼠肠系膜床灌注压力作用的介质。
Zotero 插件