Fredholm B B, Hedqvist P
Br J Pharmacol. 1978 Oct;64(2):239-45. doi: 10.1111/j.1476-5381.1978.tb17295.x.
1 Rabbit kidneys were isolated and perfused with Tyrode solution. Release of 3H-purines was studied after labeling of the adenine-nucleotide stores with [3H]adenine (more than 60% uptake during a single passage). 2 One hour after labelling the spontaneous 3H-outflow amounted to 0.1 to 0.2% of the total tissue content per minute. The release rate was enhanced following nerve stimulation (3 to 10 Hz), or brief infusion of noradrenaline (0.1 to 2.4 microgram i.a.). Release of radioactivity was also enhanced by angiotensin II, by interruption of perfusion flow for 0.5 to 2 min and by hypoxia (5 to 25% O2). 3 The release of tracer induced by nerve stimulation or noradrenaline was markedly reduced or abolished by phenoxybenzamine, which also inhibited the vasoconstrictor response. The release following angiotensin II, ischaemia and hypoxia could not be antagonized by this alpha-adrenoceptor antagonist. 4 the radioactivity in the kidney was predominantly in nucleotide form, while that released was composed mainly of nucleosides, of which adenosine predominated. 5 The results indicate that in the rabbit kidney vasocontriction, arterial clamping or reduced perfusion oxygen tension, cause release of adenosine and related compounds. In view of the reported actions of adenosine on noradrenaline effects and release in the kidney a possible physiological role is discussed.
分离兔肾并用台氏液灌注。在用[³H]腺嘌呤标记腺嘌呤核苷酸储备（单次灌注期间摄取超过60%）后，研究³H-嘌呤的释放。
标记后1小时，自发的³H流出量为每分钟总组织含量的0.1%至0.2%。神经刺激（3至10Hz）或短暂输注去甲肾上腺素（0.1至2.4微克，动脉内注射）后，释放速率加快。血管紧张素II、灌注流中断0.5至2分钟以及缺氧（5%至25%氧气）也会增强放射性的释放。
神经刺激或去甲肾上腺素诱导的示踪剂释放被酚苄明显著降低或消除，酚苄明也抑制血管收缩反应。血管紧张素II、缺血和缺氧后的释放不能被这种α-肾上腺素能受体拮抗剂拮抗。
肾中的放射性主要以核苷酸形式存在，而释放的放射性主要由核苷组成，其中腺苷占主导。
结果表明，在兔肾中，血管收缩、动脉夹闭或灌注氧张力降低会导致腺苷及相关化合物的释放。鉴于已报道的腺苷对去甲肾上腺素作用及在肾中释放的影响，讨论了其可能的生理作用。
