Karachentseva O V, Yartsev V N, Dvoretskii D P
Circulatory Physiology Laboratory, I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, 6 Makarov Bank, 199034, St. Petersburg, Russia.
Neurosci Behav Physiol. 2009 Feb;39(2):161-6. doi: 10.1007/s11055-009-9113-y. Epub 2009 Jan 13.
Experiments on isolated segments of the tail artery from young (aged 4-6 weeks) rats addressed the effects of noradrenaline (0.01-1.0 microM) on the reactions of these segments to stimulation with an electric field in isometric conditions. These studies showed that noradrenaline increases this reaction after spontaneous or acidosis (pH 6.6)-induced decreases and that the extent of this increase was proportional to the magnitude of the previous reduction in the reaction. The increase in the decrease in the reaction to electrical stimulation was accompanied by widening of the range of potentiating noradrenaline concentrations and an increase in the noradrenaline concentration at which potentiation was maximal. The nitric oxide synthesis blocker NG-nitro-L-arginine did not eliminate the potentiating effect of noradrenaline. These data led to the conclusion that noradrenaline produces a concentration-dependent recovery of decreased neurogenic reactivity of blood vessels and that this effect is not associated with changes in nitric oxide synthesis.
对幼年(4 - 6周龄)大鼠尾动脉离体节段进行的实验,研究了去甲肾上腺素(0.01 - 1.0微摩尔)在等长条件下对这些节段电场刺激反应的影响。这些研究表明,去甲肾上腺素在自发或酸中毒(pH 6.6)诱导反应降低后会增强这种反应,且这种增强的程度与之前反应降低的幅度成正比。对电刺激反应降低的增加伴随着去甲肾上腺素增强浓度范围的拓宽以及增强作用最大时去甲肾上腺素浓度的增加。一氧化氮合成阻滞剂NG - 硝基 - L - 精氨酸并未消除去甲肾上腺素的增强作用。这些数据得出结论:去甲肾上腺素可使血管降低的神经源性反应性产生浓度依赖性恢复,且这种效应与一氧化氮合成的变化无关。