Hellström P M
Acta Physiol Scand. 1987 Apr;129(4):549-56. doi: 10.1111/j.1748-1716.1987.tb08096.x.
Neuropeptide Y (NPY) and noradrenaline are suggested to coexist as neurotransmitters in sympathetic neurons. The present study investigated the mechanisms involved in the colonic vasoconstriction and inhibition of motility induced by infusion of NPY and noradrenaline close i.a. Colonic blood flow was monitored using a drop recorder, and motility was registered by a volume recording device, both operating an ordinate writer. Colonic motility was stimulated either by electrical stimulation of the pelvic nerves (PNS; 4 Hz, 5 ms, 8 V) acting via enteric ganglia or by i.v. infusion of bethanechol (10 nmol kg-1 min-1) acting directly on muscarinic receptors on smooth muscle. With both types of motility stimulation, an immediate colonic vasodilatation was registered. Electrical stimulation of the lumbar colonic nerves (4 Hz, 5 ms, 8 V) induced colonic smooth muscle relaxation and vasoconstriction during continuous PNS (P less than 0.05). Colonic contraction induced by PNS (P less than 0.01) was dose-dependently reduced by NPY (50-400 pmol min-1; P less than 0.05-0.01) and noradrenaline (1000-6000 pmol min-1; P less than 0.05-0.01). Simultaneously, vasoconstriction was induced by both NPY and noradrenaline (P less than 0.01). Colonic contraction induced by infusion of bethanechol (P less than 0.01) was not inhibited by NPY (50-200 pmol min-1). However, at the highest dose (400 pmol min-1) the motility response was reduced (P less than 0.05). Similarly, noradrenaline only at the highest dose (6000 pmol min-1) reduced the contractile response (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
神经肽Y（NPY）和去甲肾上腺素被认为在交感神经元中作为神经递质共存。本研究调查了在结肠内动脉附近输注NPY和去甲肾上腺素所诱导的结肠血管收缩和运动抑制的相关机制。使用点滴记录仪监测结肠血流，并用容积记录装置记录运动情况，二者均连接纵坐标记录仪。通过电刺激盆神经（PNS；4Hz，5ms，8V）经肠神经节起作用或静脉输注氨甲酰甲胆碱（10nmol·kg⁻¹·min⁻¹）直接作用于平滑肌上的毒蕈碱受体来刺激结肠运动。在这两种运动刺激方式下，均记录到结肠立即出现血管舒张。在持续的PNS期间，电刺激腰结肠神经（4Hz，5ms，8V）诱导结肠平滑肌舒张和血管收缩（P<0.05）。PNS诱导的结肠收缩（P<0.01）被NPY（50 - 400pmol·min⁻¹；P<0.05 - 0.01）和去甲肾上腺素（1000 - 6000pmol·min⁻¹；P<0.05 - 0.01）剂量依赖性地减弱。同时，NPY和去甲肾上腺素均诱导血管收缩（P<0.01）。氨甲酰甲胆碱输注诱导的结肠收缩（P<0.01）未被NPY（50 - 200pmol·min⁻¹）抑制。然而，在最高剂量（400pmol·min⁻¹）时运动反应减弱（P<0.05）。同样，去甲肾上腺素仅在最高剂量（6000pmol·min⁻¹）时降低收缩反应（P<0.01）。（摘要截选至250词）
