Yoshida M, Akaike T, Goto S, Takahashi W, Inadome A, Yono M, Seshita H, Maeda H, Ueda S
Department of Urology, Kumamoto University School of Medicine, Honjo, Japan.
Life Sci. 1998;62(3):203-11. doi: 10.1016/s0024-3205(97)01088-6.
In the present study, we investigated the effect of a nitric oxide (NO) scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide [carboxy-PTIO], on endothelium-dependent relaxation of a series of blood vessels from rabbits, such as thoracic aorta and femoral, renal, mesenteric, and pulmonary arteries, using a functional muscle bath technique. Carboxy-PTIO produced concentration-dependent contractions in various vessels. The contractile responses in renal, mesenteric, and pulmonary arteries were significantly greater than those in the aorta and femoral artery. Similarly, phenylephrine-induced contractions in renal, mesenteric, and pulmonary arteries were markedly enhanced after pretreatment with carboxy-PTIO. Also, carboxy-PTIO inhibited acetylcholine-induced relaxation in various blood vessels. The maximum inhibitions in aorta and femoral artery were significantly greater than those in renal, mesenteric, and pulmonary arteries. The present data demonstrate that carboxy-PTIO reduces basal, phenylephrine-, and acetylcholine-induced release of NO in rabbit blood vessels. However, different degrees of inhibition of endothelium-dependent vasorelaxation were observed in various vessels. Specifically, the thoracic aorta and femoral artery are less susceptible to the action of carboxy-PTIO without acetylcholine than renal, mesenteric, and pulmonary arteries. Conversely, the most potent carboxy-PTIO-induced inhibition of acetylcholine-induced vasorelaxation was observed with aorta and femoral arteries. Thus, it is suggested that the contribution of endogenous NO to vascular tone and regional blood flow may vary among different rabbit blood vessels.
在本研究中,我们使用功能性肌肉浴技术,研究了一氧化氮(NO)清除剂2-(4-羧基苯基)-4,4,5,5-四甲基咪唑啉-1-氧基3-氧化物[羧基-PTIO]对兔一系列血管(如胸主动脉、股动脉、肾动脉、肠系膜动脉和肺动脉)内皮依赖性舒张的影响。羧基-PTIO在各种血管中产生浓度依赖性收缩。肾动脉、肠系膜动脉和肺动脉的收缩反应明显大于主动脉和股动脉。同样,用羧基-PTIO预处理后,去氧肾上腺素诱导的肾动脉、肠系膜动脉和肺动脉收缩明显增强。此外,羧基-PTIO抑制各种血管中乙酰胆碱诱导的舒张。主动脉和股动脉中的最大抑制作用明显大于肾动脉、肠系膜动脉和肺动脉。本研究数据表明,羧基-PTIO可减少兔血管中基础状态、去氧肾上腺素和乙酰胆碱诱导的NO释放。然而,在各种血管中观察到内皮依赖性血管舒张的抑制程度不同。具体而言,在没有乙酰胆碱的情况下,胸主动脉和股动脉比肾动脉、肠系膜动脉和肺动脉对羧基-PTIO的作用更不敏感。相反,在主动脉和股动脉中观察到羧基-PTIO对乙酰胆碱诱导的血管舒张的抑制作用最强。因此,提示内源性NO对血管张力和局部血流的贡献在不同的兔血管中可能有所不同。