一氧化氮在青蛙食管体与电场刺激关系中作用的证据。

Evidence for a role for nitric oxide in relation of the frog oesophageal body to electrical field stimulation.

作者信息

Williams S J, Parsons M E

机构信息

Biosciences Division, University of Hertfordshire.

出版信息

Br J Pharmacol. 1997 Sep;122(1):179-85. doi: 10.1038/sj.bjp.0701298.

DOI:10.1038/sj.bjp.0701298

PMID:9298545

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1564890/

Abstract

Electrical field stimulation (EFS) (1-10 Hz, 30 V, 2 ms) of frog oesophageal body strips resulted in frequency-dependent non-adrenergic, non-cholinergic (NANC) relaxations. 2. Tetrodotoxin (TTX) (10(-6)-10(-5) M) had no effect on EFS evoked relaxations with a 2 ms pulse width. At a pulse width of 0.5 ms only the responses to the highest frequency (10 Hz) were significantly inhibited by TTX at 10(-5) M. Relaxation at 2 ms pulse width were unaffected by omega-conotoxin (10(-6) M), nifedipine (10(-6) M) or cobalt (5 x 10(-4) M). 3. NG-nitro-L-arginine (L-NOARG) (10(-6)-10(-4) M), a nitric oxide synthase (NOS) inhibitor, caused a concentration-dependent inhibition of the EFS-induced NANC relaxant responses. The inhibitory effect of L-NOARG was both prevented and reversed by L-arginine but not D-arginine (5 x 10(-3) M). 4. The phosphodiester type V inhibitor (PDE V), SK&F 96231 (10(-7)-10(-4) M), caused a concentration-dependent potentiation of both the percentage relaxation and the duration of the relaxant responses to EFS. 5. ODQ (10(-7)-10(-5) M), a guanylate cyclase inhibitor, produced a concentration-dependent inhibition of EFS-evoked NANC relaxations. 6. Oxyhaemoglobin (10(-6) M), which binds nitric oxide (NO), inhibited NANC relaxations to EFS. 7. The NO donor sodium nitroprusside (SNP) (10(-8)-10(-4) M) produced a concentration-dependent inhibition of evoked tone. L-NOARG (10(-4) M) had no effect on the SNP evoked relaxations. Preincubation with oxyhaemoglobin (10(-6) M) caused a reduction in the SNP (10(-6)-10(-5) M) induced relaxations. 8. These results suggest NO is the relaxant transmitter of the frog oesophageal body and the source of NO may be non-neuronal.

摘要

对蛙食管体条进行电场刺激（EFS）（1 - 10赫兹，30伏，2毫秒）可导致频率依赖性非肾上腺素能、非胆碱能（NANC）舒张。2. 河豚毒素（TTX）（10⁻⁶ - 10⁻⁵摩尔/升）对脉冲宽度为2毫秒的EFS诱发的舒张无影响。在脉冲宽度为0.5毫秒时，仅对最高频率（10赫兹）的反应在10⁻⁵摩尔/升的TTX作用下受到显著抑制。2毫秒脉冲宽度下的舒张不受ω - 芋螺毒素（10⁻⁶摩尔/升）、硝苯地平（10⁻⁶摩尔/升）或钴（5×10⁻⁴摩尔/升）的影响。3. 一氧化氮合酶（NOS）抑制剂NG - 硝基 - L - 精氨酸（L - NOARG）（10⁻⁶ - 10⁻⁴摩尔/升）对EFS诱导的NANC舒张反应产生浓度依赖性抑制。L - 精氨酸可预防并逆转L - NOARG的抑制作用，而D - 精氨酸（5×10⁻³摩尔/升）则无此作用。4. 磷酸二酯酶V型抑制剂（PDE V）SK&F 96231（10⁻⁷ - 10⁻⁴摩尔/升）对EFS诱发舒张反应的舒张百分比和舒张持续时间均产生浓度依赖性增强作用。5. 鸟苷酸环化酶抑制剂ODQ（10⁻⁷ - 10⁻⁵摩尔/升）对EFS诱发的NANC舒张产生浓度依赖性抑制。6. 能结合一氧化氮（NO）的氧合血红蛋白（10⁻⁶摩尔/升）抑制对EFS的NANC舒张。7. NO供体硝普钠（SNP）（10⁻⁸ - 10⁻⁴摩尔/升）对诱发的张力产生浓度依赖性抑制。L - NOARG（10⁻⁴摩尔/升）对SNP诱发的舒张无影响。预先用氧合血红蛋白（10⁻⁶摩尔/升）孵育会使SNP（10⁻⁶ - 10⁻⁵摩尔/升）诱导的舒张减弱。8. 这些结果表明NO是蛙食管体的舒张递质，且NO的来源可能是非神经元性的。