Release of 3H-purines from [3H]-adenine labelled rabbit kidney following sympathetic nerve stimulation, and its inhibition by alpha-adrenoceptor blockage.
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.
Release of 3H-purines from [3H]-adenine labelled rabbit kidney following sympathetic nerve stimulation, and its inhibition by alpha-adrenoceptor blockage. 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.