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Vol. 283, Issue 1, 177-182, 1997
Center for Clinical Pharmacology, University of Pittsburgh Medical
Center, Pittsburgh, Pennsylvania
We recently demonstrated that cAMP added to the perfusate increased the
renal venous recovery of adenosine in the isolated rat kidney, an
effect blocked by inhibition of ecto-phosphodiesterase and
ecto-5
-nucleotidase. Although our previous study established the
cAMP-adenosine pathway, i.e., the conversion of cAMP to
adenosine, as a viable metabolic pathway within the kidney, that study
did not determine whether conversion of arterial cAMP to adenosine recoverable in the venous effluent occurred in the tubules
versus nontubular sites. In the current study, we
addressed this issue by determining the effects of blocking cAMP
transport into the renal tubules with probenecid (0.1, 0.3 and 1 mM) on
the increase in renal venous output of adenosine induced by adding cAMP
(30 µM) to the perfusate of isolated rat kidneys. Addition of cAMP to
the perfusate caused a marked increase in renal venous secretion of
adenosine, an effect that was augmented, rather than inhibited, by
probenecid. To test the hypothesis that the renal vasculature supports
a cAMP-adenosine pathway, cultured rat preglomerular vascular smooth
muscle cells were incubated with cAMP (30 µM) for 1 hr in the
presence and absence of 3-isobutyl-1-methylxanthine (a
phosphodiesterase inhibitor). Incubation with cAMP increased extracellular adenosine levels 41-fold, and this effect was abolished by 3-isobutyl-1-methylxanthine. In a third experimental series, addition of cAMP (0.3, 1, 3, 10 and 30 µM) to the perfusate of isolated rat kidneys and mesenteric vascular beds increased the renal
venous, but not mesenteric venous, output of AMP, adenosine and
inosine. We conclude that the renal vasculature supports a cAMP-adenosine pathway, that administering cAMP into the renal artery
and measuring adenosine in the venous effluent of the perfused rat
kidney most likely monitors primarily the renal vascular cAMP-adenosine pathway and that the quantitative importance of the cAMP-adenosine pathway is not equivalent in all vascular compartments.
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