Effect of allopurinol on the renovascular responses to adenosine
Macias-Nunez, J.F.; Revert, M.; Fiksen-Olsen, M.; Knox, F.G.; Romero, J.C.
Journal of Laboratory and Clinical Medicine 108(1): 30-36
1986
ISSN/ISBN: 0022-2143 PMID: 3519811 Document Number: 281241
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 per hour to 3.8 .+-. 0.4 ng/ml per 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 per hour and 8.2 .+-. 0.6 ng/ml per 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.