Key result
Dipyridamole potently inhibits saturable pulmonary cellular adenosine uptake and nucleotide incorporation.
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Adenosine uptake was studied in the piglet isolated perfused lung by means of the single-circulation paired-tracer dilution technique. Adenosine was efficiently taken up from the pulmonary vascular bed, and the process was potently inhibited by dipyridamole. Following uptake, adenosine was incorporated into intracellular nucleotides, and at low perfusate concentrations, little or none of the incorporated radioactivity returned to the circulation. At higher concentrations, cellular uptake was saturable and products of intracellular catabolism (inosine and hypoxanthine) were returned to the circulation. Perfusion of low concentrations of adenosine after inhibition of pulmonary adenosine kinase led to a proportional decrease in the retention of nucleotides and to a release of inosine and hypoxanthine. A small proportion of adenosine was metabolised extracellularly by adenosine deaminase; this activity was not released from perfused lungs and is apparently an ecto-enzyme.
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Hellewell et al. (1983) studied this question. Adenosine perfusion (with dipyridamole or adenosine kinase inhibition) was evaluated on Pulmonary vascular adenosine uptake and metabolism into intracellular nucleotides, inosine, and hypoxanthine. Adenosine perfusion in isolated piglet lungs showed saturable cellular uptake into nucleotides that was potently inhibited by dipyridamole.
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