Dopamina renal: nuevos roles con implicancias clínicas en nefroprotección y regulación de la presión arterial

Renal dopamine (DA) regulates water and sodium excretion and, doing so, controls blood pressure. Renal epithelial cells produce DA by decarboxylation of filtered l-dopa and inactivate DA by monoamineoxidase (MAO) and catechol-O-methyl transferase (COMT). Dopamine interacts with specific receptors (D1R and D2R). The aim of this work is to study urinary DA excretion (UDA*V) and MAO and COMT activities in rats under different sodium intake. Four groups according to Na+ intake and treatment were studied: Normal (NS, NaCl 0.24%), Low (BS, 0.02%) and High sodium (HS, 1%) for 5 days. In group four, NS, BS and HS rats received SCH 23390 (1 mg/kg SC), D1R antagonist, the last three days. Results: UDA*V (ng/d/100g bwt) was lower in BS 571±30 vs NS 730±45, p< 0.01 and was increased in HS to 1443±203 p<0.01vs NS and p<0.001 vs BS. In BS rats MAO activity (nmol/mg/h) increased in renal cortex to 9.44±0.55 vs NS 7.66±0.52, p<0.05, while MAO decreased in HS cortex to 6.3±0.25, p<0.05 vs NS. COMT activity (pmol/mg/h), increased in cortex of BS rats to 15.67±1.23 vs 11.04±0.13 in NS group, p<0.05. Regardless Na+ intake, MAO was always higher in cortex than in renal medulla, while COMT did not show differences between cortex and medulla. SCH 23390 markedly decreased diuresis and natriuresis in HS rats and Na+ excretion in NS and increased systolic pressure in BS. Conclusion: dopamine and Na+ excretion are positively related to Na+ intake. MAO and COMT are involved in this response mainly mediated by D1R stimulation.