Adenosine does not mediate renal sodium retention and peripheral vasodilation elicited by partial portal vein ligation in rats

This study was conducted to assess the role of adenosine in the peripheral vasodilation and sodium retention that occurs after partial portal vein ligation (PVL) in the rat. The experiment was performed on day 1 after surgery when transient maximal sodium retention developed and day 7 when rats returned to sodium balance. Hemodynamic studies were conducted under anesthesia in portal hypertensive rats with sodium retention and in sham‐operated controls. Measurements were obtained before and after administration of a nonselective A1 and A2 adenosine receptor antagonist 1,3‐dipropyl‐8‐p‐sulfophenylxanthine (DPSPX) (10 mg/kg intravenously followed by 150 μg/min). Under baseline conditions, portal hypertensive rats with sodium retention were hypotensive, with decreases in total peripheral resistance and filtration fraction on day 1 in comparison with the control group. Although hyperdynamic circulation was still maintained by day 7, there was a return to sodium balance. The adenosine receptor antagonist had a modest vasoconstrictor effect on systemic and renal vasculature in both groups, but less in portal hypertensive rats. However, no change in glomerular filtration rate was observed. DPSPX induced a natriuresis in control rats (from 0.40 ± 0.11 to 5.97 ± 0.61 mEq/min on day 1, from 0.48 ± 0.20 to 6.34 ± 0.45 mEq/min on day 7). This response was attenuated in portal hypertensive rats on day 1 (from 0.14 ± 0.04 to 1.67 ± 0.57 mEq/min), but not on day 7 (from 0.20 ± 0.06 to 5.11 ± 0.55 mEq/min). These results suggest that in portal hypertensive rats (1) adenosine is not responsible for vasodilation and sodium retention, (2) a sodium‐retaining factor acting directly on the renal tubule is responsible for sodium retention.