Neither a purine nor VIP is the mediator of inhibitory nerves of opossum oesophageal smooth muscle.

Neither a purine nor VIP is the mediator of inhibitory nerves of opossum oesophageal smooth muscle.
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嘌呤和VIP都不是负鼠食管平滑肌抑制神经的介质。

DOI:
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发表时间:
1983
期刊:
Journal of Physiology
影响因子:
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通讯作者:
M. Kannan
M. Kannan
中科院分区:
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文献类型:
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作者:
E. Daniel;A. Helmy;L. Jager;M. Kannan

文献摘要

被引文献

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研究了负鼠(Didelphis marsupialis)食道体圆形平滑肌层壁内神经刺激的效果,同时使用蔗糖间隙法测量肌肉细胞的膜电位和肌肉收缩。在27℃下,用克雷布斯溶液对该制剂进行电场刺激,诱导平滑肌细胞膜(i.j.p)的瞬态超极化,随后是肌肉动作电位叠加的瞬态去极化。肌肉不自发产生主动张力;因此,在“关闭”去极化期间,它并没有放松,而是经常收缩。i.j.p.及其反应的特点是由内源性、非肾上腺素能、非胆碱能(n.a.n.c)神经介导。提高外源钾浓度可降低i.j.p.振幅。当氯离子被异硫代酸盐取代时,平滑肌细胞膜出现小的超极化,同时i.j.p.振幅也有相应的小幅度降低。在无Cl - free培养基中,ijp后的“off”活性完全消失。Apamin(10(‐7)‐10(‐5)M)不影响该制备,也不影响i.j.p。浓度高达10(‐3)M的腺苷及其相关腺嘌呤核苷酸几乎不影响制备。外源性血管活性肠多肽(VIP)诱导平滑肌细胞膜节律性去极化和自发收缩,这些对神经毒素不敏感,但在无氯介质中不存在。在VIP存在的情况下,现场刺激引起了i.j.p.,短暂地中断了VIP诱导的收缩反应。结果表明,负鼠食道圆形平滑肌层内神经的抑制介质既不是嘌呤,也不是VIP。这可能是由于平滑肌细胞膜钾离子通透性的选择性增加,而“关闭”去极化可能与Cl离子电导率的增加有关。这表明,神经递质的释放是通过P1 -嘌呤受体突触前调节的,VIP可能是一种兴奋性递质,与抑制性递质同时释放。
Effects of stimulation of intramural nerves in the circular smooth muscle layer of the body of the oesophagus of the opossum (Didelphis marsupialis) were studied, simultaneously measuring the membrane potential of muscle cells using the sucrose‐gap technique and contractions of the muscle. Electrical field stimulation of the preparation, superfused with Krebs solution at 27 degrees C, induced a transient hyperpolarization of the smooth muscle cell membrane (i.j.p.) followed by a transient depolarization on which muscle action potentials were often superimposed. The muscle did not develop active tension spontaneously; it therefore did not relax during the i.j.p., but often contracted during the ‘off’ depolarization. The i.j.p. and the responses following it were characterized as mediated by intramural, non‐adrenergic, non‐cholinergic (n.a.n.c.) nerves. The i.j.p. amplitude was reduced by raising the external K concentration. When Cl was replaced by isethionate, a small hyperpolarization of the smooth muscle cell membrane ensued along with a comparable small reduction of the i.j.p. amplitude. The ‘off’ activity following the i.j.p. disappeared completely in Cl‐free medium. Apamin (10(‐7)‐10(‐5) M) did not influence this preparation nor the i.j.p. Adenosine and its related adenine nucleotides in concentrations up to 10(‐3) M hardly affected the preparation. Prolonged superfusion with adenosine and 6‐chloroadenosine revealed a gradually increasing attenuation of the i.j.p. Exogenously applied vasoactive intestinal polypeptide (VIP) induced rhythmic depolarizations of the smooth muscle cell membrane and spontaneous contractions, which were insensitive to neurotoxins but absent in Cl‐free media. Field stimulation in the presence of VIP caused an i.j.p. which transiently interrupted the VIP‐induced contractile responses. It is concluded that the inhibitory mediator of the intramural n.a.n.c. nerves present in the circular smooth muscle layer of the opossum oesophagus is neither a purine nor VIP. The i.j.p. may result from a selective increase in K permeability of the smooth muscle cell membrane, the ‘off’ depolarization may involve an increase in the Cl ion conductance. The suggestion is made that the release of neurotransmitter from intramural n.a.n.c. nerves is modulated presynaptically via P1‐purinoceptors and that VIP is a likely candidate for an excitatory transmitter, released simultaneously with the inhibitory transmitter.