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绵羊膀胱颈肌肉非肾上腺素能非胆碱能(NANC)刺激后(“反弹”)收缩的特征

Characteristics of the NANC post-stimulus ('rebound') contraction of the urinary bladder neck muscle in sheep.

作者信息

Thornbury K D, Donaghy K M, Peake J

机构信息

Department of Physiology, School of Biomedical Science, Queen's University of Belfast, Northern Ireland.

出版信息

Br J Pharmacol. 1995 Nov;116(5):2451-6. doi: 10.1111/j.1476-5381.1995.tb15095.x.

Abstract
  1. Strips of muscle from sheep bladder neck were set up for tension recording and subjected to electrical field stimulation (EFS) to stimulate their intramural nerves. 2. In the presence of atropine (1 microM) and guanethidine (1 microM), the response to 1 Hz EFS was biphasic, characterized by a relaxation during the stimulus period, followed by a post-stimulus contraction. A similar biphasic response was also seen following bolus application of nitric oxide (NO). 3. In the absence of atropine and guanethidine, the relaxations were masked by contractions during stimulation; however, the post-stimulus contraction were unaffected. L-NAME (100 microM) blocked the post-stimulus contractions and L-arginine (1 mM) restored them, suggesting that they were NO-mediated. 4. M&B 22948, a phosphodiesterase inhibitor, prolonged the relaxations and abolished the post-stimulus contractions. This suggests that rapid removal of cyclic GMP is required for post-stimulus contraction to occur. 5. When the number of pulses in the stimulus train was kept constant, the size of the post-stimulus contraction increased as the duration of the preceding period of stimulation increased. Maximal post-stimulus contractions were obtained following stimulation for > 40 s. 6. The L-channel antagonist, nifedipine (1 microM) and verapamil (1 microM), had little effect on the amplitude of the post-stimulus contractions. 7. In contrast, ryanodine-(8 microM) reduced the post-stimulus contractions by over 90%. Caffeine (20 mM) also abolished the post-stimulus contractions and cyclopiazonic acid (CPA, 10 microM) reduced them by 76%. However, in the presence of CPA a slower post-stimulus contraction developed. Nifedipine (1 microM) reduced this by 40%. 8. In conclusion, these results support a role for NO in the post-stimulus contraction of the sheep bladder neck muscle. The post-stimulus contraction depends more on release of intracellular Ca2+, than Ca2+ influx through L-type channels.
摘要
  1. 取绵羊膀胱颈的肌肉条进行张力记录,并施加电场刺激(EFS)以刺激其壁内神经。2. 在阿托品(1微摩尔)和胍乙啶(1微摩尔)存在的情况下,对1赫兹EFS的反应呈双相性,其特征为刺激期出现松弛,随后是刺激后收缩。在一次性应用一氧化氮(NO)后也观察到类似的双相反应。3. 在没有阿托品和胍乙啶的情况下,刺激期间的松弛被收缩掩盖;然而,刺激后收缩不受影响。L-硝基精氨酸甲酯(L-NAME,100微摩尔)阻断刺激后收缩,L-精氨酸(1毫摩尔)使其恢复,这表明它们是由NO介导的。4. 磷酸二酯酶抑制剂M&B 22948延长了松弛时间并消除了刺激后收缩。这表明刺激后收缩的发生需要快速清除环磷酸鸟苷(cGMP)。5. 当刺激串中的脉冲数保持恒定时,刺激后收缩的大小随着先前刺激期持续时间的增加而增加。刺激超过40秒后可获得最大刺激后收缩。6. L型通道拮抗剂硝苯地平(1微摩尔)和维拉帕米(1微摩尔)对刺激后收缩的幅度影响很小。7. 相比之下,ryanodine(8微摩尔)使刺激后收缩减少超过90%。咖啡因(20毫摩尔)也消除了刺激后收缩,环匹阿尼酸(CPA,10微摩尔)使其减少76%。然而,在CPA存在的情况下,出现了较慢的刺激后收缩。硝苯地平(1微摩尔)使其减少40%。8. 总之,这些结果支持NO在绵羊膀胱颈肌肉刺激后收缩中起作用。刺激后收缩更多地依赖于细胞内Ca2+ 的释放,而不是通过L型通道的Ca2+ 内流。

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