Adenosine is a potent endogenous renal vasoconstrictor. To investigate the sensitivity of the renal circulation to adenosine in cirrhosis, we evaluated kidney function and vasoactive hormones in 20 patients with cirrhosis before and after administration of dipyridamole (0.4 mg/kg, intravenously), a drug that increases extracellular levels of adenosine. In patients with ascites and increased plasma renin activity (6.9 ± 4.0 ng/ml hr [mean ± S.D.]) (n = 7), dipyridamole induced marked reductions in renal plasma flow (from 623 ± 294 to 374 ± 188 ml/min, p = 0.03), glomerular filtration rate (from 89 ± 22 to 48 ± 16 ml/min, p = 0.009), urine volume (from 7.1 ± 2.1 to 1.5 ± 1.1 ml/min, p = 0.0001), free water clearance (from 4.0 ± 1.7 to 0.4 ± 0.6 ml/min, p = 0.001) and sodium excretion (from 28 ± 36 to 7 ± 15 μEq/min, p = 0.05) in the absence of changes in arterial pressure, plasma renin activity and levels of aldosterone, norepinephrine and antidiuretic hormone. In patients without ascites (n = 5) and in patients with ascites and normal plasma renin activity (0.9 ± 0.5 ng/ml hr) (n = 8), renal plasma flow and glomerular filtration rate did not change significantly after dipyridamole administration, whereas excretion of sodium and free water was reduced. These results indicate that in cirrhotic patients with ascites and overactivity of the renin-angiotensin system, dipyridamole induces renal vasoconstriction in the absence of changes in systemic hemodynamics, suggesting that these patients are particularly sensitive to the renal vasoconstrictor effect of endogenous adenosine. (HEPATOLOGY 1993;17:59–64.)
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