Adenosine activates aromatic L-amino acid decarboxylase activity in the kidney and increases dopamine

Renal sodium handling is important for regulating BP, and renal dopamine an d adenosine play an important role in renal sodium handling, however the in teraction of these hormones in the kidney was not clarified. In in vivo exp eriments, adenosine significantly increased water and sodium excretion by 5 0% compared with vehicle when infused into the left renal artery, accompani ed by an increase in urinary dopamine excretion in the left kidney. Neither water-sodium excretion nor dopamine excretion changed in the vehicle-infus ed kidney. Aromatic L-amino acid decarboxylase activity in the left kidney was significantly higher than that in the noninfused right kidney. The incr ease in water-sodium excretion induced by adenosine was significantly inhib ited by SCH23390, a selective D1 receptor antagonist. In in vitro experimen ts, porcine renal proximal tubular cells were incubated with 250 muM L-dopa and Nb-cyclohexyladenosine, an adenosine type 1 receptor agonist, after tr eatment with adenosine deaminase. N-6-cyclohexyladenosine significantly inc reased dopamine formation at a concentration of 10(-9) to 10(-7) M, and thi s was completely inhibited by 1,3-dipropyl-8-cyclopentylxanthin, an adenosi ne A1 antagonist. These results show that renal dopamine synthesis is stimu lated by adenosine through the activation of aromatic L-amino acid decarbox ylase and suggest that adenosine leads to an increase in renal dopamine and natriuresis.