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Abstract
It is known that renal ischemia enhances the production of adenosine, which is further
metabolized by xanthine oxidase, and that the inhibition of this metabolizing enzyme
by allopurinol ameliorates the consequences of renal ischemia. This study was undertaken
to define the effect of allopurinol on the renal responses to adenosine. It was found
that 5 minutes of intrarenal infusion of adenosine in control dogs produced a typical
biphasic response characterized by an initial vasoconstriction, decreasing renal blood
flow by 46.3% ± 6.0%, followed by vasodilatation, increasing renal blood flow by 8.5%
± 3.6% above the control levels. Adenosine infusion was also accompanied by a significant
reduction of plasma renin activity, from 8.4 ± 0.6 ng/ml/hour to 3.8 ± 0.4 ng/ml/hour.
The administration of an intravenous infusion of 50 mg allopurinol did not alter the
vasoconstrictor phase of adenosine—the average decrease was 41.1% ± 3.3%; however,
it prevented much of the vasodilatation because renal blood flow over the 5 minutes
remained 17.9% ± 5.0% less than the levels recorded before adenosine infusion. Allopurinol
also prevented the decrease of plasma renin activity, for which the average values
recorded before and after adenosine were 9.6 ± 0.6 ng/ml/hour and 8.2 ± 0.6 ng/ml/hour,
respectively. The results of this study indicate that allopurinol exerts specific
effects on the vasodilatory component of adenosine and prevents the adenosine-suppressive
effect on the renin-angiotensin system.
Abbreviations:
ADP (adenosine diphosphate), AMP (adenosine monophosphate), ATP (adenosine triphosphate)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
March 26,
1986
Received:
March 19,
1986
Footnotes
☆Supported in part by Research Grants HL-16496 and HL-14133 from the National Institutes of Health and by Grant 3482728 from Mayo Foundation.
Identification
Copyright
© 1986 Published by Elsevier Inc.
