Changes of adenosine levels in the carotid artery, renal vein and inferior vena cava after glycerol or mercury injection in the rat.

The adenosine A1 receptor antagonist (FR113453) prevents glycerol- but not mercury-induced acute renal failure. To clarify this mechanism, adenosine concentration in the renal vein was measured serially. Plasma adenosine in the renal vein increased from the preinjection value of 120.6 +/- 15.4 (mean +/- SEM) pmol/ml to 426.9 +/- 107.5, 407.0 +/- 70.1 and 283.9 +/- 22.9 pmol/ml at 1, 5 and 60 min after intramuscular injection of 10 mg/kg of 50% glycerol into Sprague-Dawley rats. On the other hand, intramuscular vehicle (0.9% NaCl) injection and subcutaneous administration of 10 mg/kg of HgCl2 did not change or caused mild elevation of adenosine concentration in the renal vein. Furthermore, simultaneous blood collection from the carotid artery, renal vein and inferior vena cava revealed a greater increase in adenosine concentration in the inferior vena cava than in the artery or renal vein. These findings were not affected by the administration of FR113453 or vehicle (methylcellulose). The increase in adenosine in the inferior vena cava was derived from the release from the acutely damaged muscles due to glycerol injection. These findings suggest that the effect of adenosine A1 antagonist to prevent glycerol-induced acute renal failure is due to the inhibition of adenosine A1 receptor in the kidneys during the release of adenosine through the inferior vena cava. Therefore, the release of adenosine from the muscle and hemolysis plays an important role to induce acute renal failure in the glycerol-injected rat.