Journal of Applied Physiology, Vol 65, Issue 1 297-305, Copyright © 1988 by American Physiological Society
Adenosine transport by the lung
D. K. Das and H. Steinberg
Cardiovascular Division, University of Connecticut School of Medicine, Farmington 06032.
Adenosine, a nucleoside and potent vasodilator, has been found to be taken
up by the lung and converted by deamination into inosine and hypoxanthine.
In a single circulation through an isolated rat lung, 69.3 +/- 3.3% of
infused [14C]adenosine (10 microM) was removed from the circulation. Uptake
of [14C]adenosine remained unchanged when deamination of adenosine was
inhibited by 8-azaguanine or coformycin. In a single passage of adenosine
through the pulmonary artery, very little of the deaminated products
appeared in the pulmonary circulation, but when adenosine was recirculated
through the pulmonary circulation inosine and hypoxanthine appeared in the
venous effluent. These adenosine metabolites were also taken up by the
lung. A major portion of the circulating adenosine was transported into the
lung, where it was used to synthesize adenine nucleotides. Inhibition of
adenosine kinase by iodotubercidin resulted in reduced formation of ATP and
ADP. Uptake of adenosine by the lung was saturable on a concentration
gradient and was a passive process because it was not affected by the
absence of glucose or the presence of ouabain. Km and Vmax for adenosine
transport were 0.227 mM and 4.6 mumol.min-1.g lung-1, respectively.
Adenosine transport was inhibited by adenosine analogues, and the
inhibitions were found to be competitive in nature. These results suggest
that a specific and rate-limiting transport system exists in the lung for
adenosine.
