Hedqvist P, Fredholm B B
Naunyn Schmiedebergs Arch Pharmacol. 1976 Jun;293(3):217-23. doi: 10.1007/BF00507344.
The action of adenosine on adrenergic neuroeffector transmission was studied in the rabbit kidney in vitro and in situ, in the canine subcutaneous adipose tissue in situ and in the guinea pig vas deferens in vitro. In the kidney, adenosine (0.1-10 muM) caused a concentration-dependent increase in vascular resistance and in vasoconstrictor responses to nerve stimulation and administered noradrenaline. In the adipose tissue, adenosine also increased the vaso-constrictor responses but it decreased vascular resistance. In all three tissues studied adenosine significantly and reversibly depressed noradrenaline release evoked by nerve stimulation in a concentration-dependent manner. This effect of adenosine was not altered by phenoxybenzamine which blocked all vasoconstrictor responses and diminished the rise in vascular resistance by adenosine in the kidney. It is concluded that adenosine affects adrenergic neuroeffector transmission by two discrete mechanisms, prejunctional inhibition and postjunctional enhancement.
在体外和原位兔肾、原位犬皮下脂肪组织以及体外豚鼠输精管中研究了腺苷对肾上腺素能神经效应器传递的作用。在肾脏中,腺苷(0.1 - 10 μM)引起血管阻力以及对神经刺激和给予去甲肾上腺素的血管收缩反应呈浓度依赖性增加。在脂肪组织中,腺苷也增加血管收缩反应,但降低血管阻力。在所研究的所有三种组织中,腺苷以浓度依赖性方式显著且可逆地抑制神经刺激诱发的去甲肾上腺素释放。苯氧苄胺可阻断所有血管收缩反应并减弱肾脏中腺苷引起的血管阻力升高,但腺苷的这种作用并未被其改变。得出的结论是,腺苷通过两种不同机制影响肾上腺素能神经效应器传递,即突触前抑制和突触后增强。