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 and adenosine play an important role in renal sodium handling, however the interaction of these hormones in the kidney was not clarified. In in vivo experiments, adenosine significantly increased water and sodium excretion by 50% compared with vehicle when infused into the left renal artery, accompanied by an increase in urinary dopamine excretion in the left kidney. Neither water-sodium excretion nor dopamine excretion changed in the vehicle-infused kidney. Aromatic L-amino acid decarboxylase activity in the left kidney was significantly higher than that in the noninfused right kidney. The increase in water-sodium excretion induced by adenosine was significantly inhibited by SCH23390, a selective D1 receptor antagonist. In in vitro experiments, porcine renal proximal tubular cells were incubated with 250 microM L-dopa and N(6)-cyclohexyladenosine, an adenosine type 1 receptor agonist, after treatment with adenosine deaminase. N(6)-cyclohexyladenosine significantly increased dopamine formation at a concentration of 10(-9) to 10(-7) M, and this was completely inhibited by 1,3-dipropyl-8-cyclopentylxanthin, an adenosine A1 antagonist. These results show that renal dopamine synthesis is stimulated by adenosine through the activation of aromatic L-amino acid decarboxylase and suggest that adenosine leads to an increase in renal dopamine and natriuresis.
Takezako
Takanobu
T
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
Noda
Keita
K
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
Tsuji
Emiko
E
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
Koga
Manabu
M
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
Sasaguri
Manabu
M
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
Arakawa
Kikuo
K
Department of Internal Medicine, Fukuoka University, School of Medicine, Fukuoka, Japan.
D000241:Adenosine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D001142:Aromatic-L-Amino-Acid Decarboxylases / Q000378:metabolism*; D001552:Benzazepines / Q000494:pharmacology; D004231:Diuresis / Q000187:drug effects; D004298:Dopamine / Q000378:metabolism*; D004789:Enzyme Activation / Q000187:drug effects; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism*; D018374:LLC-PK1 Cells; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D058906:Purinergic P1 Receptor Agonists; D058915:Purinergic P1 Receptor Antagonists; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors; D013552:Swine
D001552:Benzazepines; D058906:Purinergic P1 Receptor Agonists; D058915:Purinergic P1 Receptor Antagonists; D017447:Receptors, Dopamine D1; C027513:N(6)-cyclohexyladenosine; D007980:Levodopa; D001142:Aromatic-L-Amino-Acid Decarboxylases; D000241:Adenosine; D004298:Dopamine