Neild T O, Kotecha N
Department of Physiology, Monash University, Clayton, Victoria, Australia.
J Auton Nerv Syst. 1990 Apr;30(1):29-35. doi: 10.1016/0165-1838(90)90161-b.
Neuropeptide Y was applied to arterioles of the submucosa of the guinea-pig small intestine while arteriole diameter and smooth muscle membrane potential were monitored. Neuropeptide Y (50 nM-1 microM) caused no smooth muscle depolarization, and caused a small constriction in only 15 out of 38 arterioles studied. 50 nM Neuropeptide Y increased the amplitude of constriction caused by noradrenaline or brief trains of nerve stimulation, showing that it potentiated the effects of vasoconstrictors as it does in other arteries. The factor by which the amplitude was increased was greatest for small constrictions. Neuropeptide Y reduced the amplitude of the excitatory junction potential, suggesting that it decreased neurotransmitter release. These results show that the potentiating action of Neuropeptide Y does not depend on smooth muscle depolarization.
将神经肽Y应用于豚鼠小肠黏膜下小动脉,同时监测小动脉直径和平滑肌膜电位。神经肽Y(50 nM - 1 μM)未引起平滑肌去极化,在所研究的38条小动脉中,仅15条出现轻微收缩。50 nM神经肽Y增加了去甲肾上腺素或短暂串刺激引起的收缩幅度,表明它与在其他动脉中一样,增强了血管收缩剂的作用。收缩幅度增加的倍数在小收缩时最大。神经肽Y降低了兴奋性接头电位的幅度,提示它减少了神经递质的释放。这些结果表明,神经肽Y的增强作用不依赖于平滑肌去极化。