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首页> 外文期刊>The Journal of Physiology >Role of alpha(2)-adrenoceptors in the sympathetic inhibition of motility reflexes of guinea-pig ileum.
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Role of alpha(2)-adrenoceptors in the sympathetic inhibition of motility reflexes of guinea-pig ileum.

机译:α(2)-肾上腺素受体在交感抑制豚鼠回肠运动反射中的作用。

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1. Sympathetic regulation of the motility of guinea-pig ileum was investigated using mesenteric nerve (MN) stimulation to inhibit motility reflexes, in vitro. 2. Transmural electrical stimulation (5 Hz, 1 s) in intact intestinal segments, or inflation of a balloon against the mucosa in opened segments, evoked contractions of the circular and longitudinal muscles oral to the stimulus. 3. MN stimulation (10 Hz, 5 s) usually abolished contractions of the longitudinal and circular muscles evoked by either electrical or mechanical stimuli. 4. The inhibition was mimicked by UK14,304 (70-100 nM) and abolished by idazoxan (100 nM), revealing an enhancement of circular muscle contractions. There was no evidence for alpha(2)-receptors on the muscle, suggesting sympathetic inhibition was via the myenteric plexus. 5. Possible sites of action of noradrenaline released from sympathetic nerves were investigated using intracellular recordings from the circular muscle in a multichambered organ bath. 6. When in the stimulation chamber, UK14,304 depressed (by 50 %) excitatory junction potentials (EJPs) recorded oral to a distension stimulus, but did not affect inhibitory junction potentials (IJPs) recorded anal to the stimulus. When added to a chamber between the stimulus and recording chambers, UK14,304 depressed EJPs by 40 %, but did not alter IJPs. When in the recording chamber, UK14,304 depressed EJPs by 20 %, but had no effect on IJPs. IJPs were inhibited, however, when UK14,304 was applied to the whole bath. 7. It is concluded that sympathetic activity inhibits intestinal motility mainly via alpha(2)-adrenoceptors on ascending interneurons and intrinsic sensory neurons of the orally directed reflex pathway.
机译:1.使用肠系膜神经(MN)刺激体外抑制豚鼠回肠运动的交感调节。 2.在完整的肠段进行透壁电刺激(5 Hz,1 s),或在打开的段中使气球向粘膜充气,刺激口腔和纵向肌肉收缩。 3. MN刺激(10 Hz,5 s)通常消除了电刺激或机械刺激引起的纵向和环形肌肉的收缩。 4. UK14,304(70-100 nM)模仿了抑制作用,而伊达唑烷(100 nM)取消了抑制作用,显示出环形肌肉收缩的增强。没有证据表明肌肉上有α(2)-受体,表明交感神经抑制是通过肌间神经丛。 5.使用多腔器官浴中环状肌肉的细胞内记录,研究了交感神经释放去甲肾上腺素的可能作用部位。 6.在刺激室中,UK14,304记录了对扩张刺激物口服的兴奋性连接电位(EJPs)降低(降低了50%),但不影响肛门刺激物记录的抑制性接合电位(IJPs)。当UK14,304添加到刺激室和记录室之间的室中时,EJP降低了40%,但并未改变IJP。在记录室中时,UK14304将EJP降低了20%,但对IJP没有影响。但是,当将UK14,304应用于整个浴液时,IJP被抑制。 7.结论是,交感神经活动主要通过α(2)-肾上腺素受体对口服定向反射通路的上升中神经元和内在感觉神经元的抑制而抑制肠蠕动。

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