Ramme D, Regenold J T, Starke K, Busse R, Illes P
Institut für Pharmakologie, Universität Freiburg, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1987 Sep;336(3):267-73. doi: 10.1007/BF00172677.
Vasoconstriction or excitatory junction potentials (e.j.ps) evoked by nerve stimulation (15 field pulses at 2 Hz every 3 min) were recorded in rabbit isolated jejunal arteries. The resting diameter of the arteries and its decrease in response to stimulation was measured by a photoelectric method. Vasoconstriction was insensitive to prazosin 0.1 or 1 mumol/l. Yohimbine 1 mumol/l considerably enhanced, whereas alpha,beta-methylene ATP (alpha,beta-meATP) 1 mumol/l abolished the contractile response. In order to test the effect of exogenously applied transmitter candidates, noradrenaline (0.1-1 mumol/l) and ATP (10-30 mumol/l) were added in concentrations which evoked a vasoconstriction comparable to that induced by electrical stimulation. The action of noradrenaline was prevented by prazosin 0.1 mumol/l, but was unaffected by both yohimbine 1 mumol/l and alpha,beta-meATP 1 mumol/l. Alpha,beta-meATP 1 mumol/l depressed the effect of ATP. The e.j.ps evoked by a train of 15 pulses showed facilitation up to the third response and thereafter depression; a partial summation was also observed. Prazosin 0.1 mumol/l did not change the e.j.p. amplitudes. By contrast, when yohimbine 0.1 or 1 mumol/l was added to the prazosin-containing medium, both the late e.j.ps in the train and the summation were enhanced in a concentration-dependent manner. Alpha,beta-meATP 1 mumol/l almost abolished the e.j.ps. In conclusion, in rabbit jejunal arteries, stimulation of postganglionic sympathetic nerves may release noradrenaline together with ATP which is probably the sole neuroeffector transmitter under our conditions. Transmitter release seems to be modulated by the activation of presynaptic alpha 2-adrenoceptors. Under the stimulation conditions of the present experiments the released transmitter does not activate postsynaptic alpha 1-adrenoceptors.
在兔离体空肠动脉中记录神经刺激(每3分钟以2赫兹施加15个场刺激脉冲)诱发的血管收缩或兴奋性接头电位(e.j.ps)。采用光电方法测量动脉的静息直径及其对刺激的减小情况。血管收缩对0.1或1微摩尔/升的哌唑嗪不敏感。1微摩尔/升的育亨宾显著增强收缩反应,而1微摩尔/升的α,β-亚甲基ATP(α,β-meATP)则消除收缩反应。为了测试外源性应用的候选递质的作用,加入了浓度为0.1 - 1微摩尔/升的去甲肾上腺素和浓度为10 - 30微摩尔/升的ATP,其诱发的血管收缩程度与电刺激诱导的相当。0.1微摩尔/升的哌唑嗪可阻断去甲肾上腺素的作用,但1微摩尔/升的育亨宾和1微摩尔/升的α,β-meATP对其无影响。1微摩尔/升的α,β-meATP可抑制ATP的作用。由15个脉冲组成的串刺激诱发的e.j.ps在第三次反应前表现为易化,之后则为抑制;还观察到部分总和现象。0.1微摩尔/升的哌唑嗪不改变e.j.p.的幅度。相比之下,当在含哌唑嗪的培养基中加入0.1或1微摩尔/升的育亨宾时,串刺激中的晚期e.j.ps和总和现象均呈浓度依赖性增强。1微摩尔/升的α,β-meATP几乎消除了e.j.ps。总之,在兔空肠动脉中,刺激节后交感神经可能释放去甲肾上腺素和ATP,在我们的实验条件下,ATP可能是唯一的神经效应递质。递质释放似乎受突触前α2 - 肾上腺素能受体激活的调节。在本实验的刺激条件下,释放的递质不激活突触后α1 - 肾上腺素能受体。