Protein-induced increase in urinary dopamine in normal and diabetic rats: role of catecholamine precursors

Feeding and protein intake increase renal dopamine excretion (UDAV). Here the contribution of amino acids (AA), L-tyrosine (Tyr), and L-phenylalanine (Phe) to UDAV in conscious normal rats and in animals with streptozotocin (STZ)-induced (60 mg/kg) diabetes mellitus was investigated. Feeding a standard chow (17.3% protein) increased UDAV in normal rats over twofold compared with the fasted state, but the effect was completely abolished by feeding a low-protein (LP, 0.03%) diet. In STZ rats, UDAV was equal to that of normal rats during the fasted periods but was higher in fed animals, resulting most likely from the higher protein intake of STZ rats. In another series, rats on LP diet were given AA solutions (7, 14, and 21 g.kg-1.24 h-1) by gastric tube, which dose dependently increased UDAV to 67.3 +/- 4.3, 91.1 +/- 5.0, and 129 +/- 17 nmol.kg-1.day-1, respectively, compared with tap water as vehicle control (H2O, 55.6 +/- 7.0 nmol.kg-1.day-1). In rats kept without access to chow, administration of AA including Phe and Tyr (AAPT) increased UDAV twofold compared with H2O, whereas AA solution without Tyr and Phe did not change UDAV. Tyr or Phe alone increased UDAV to the same extent as observed in AAPT. Higher doses of Tyr further increased UDAV dose dependently but with saturation characteristics. UDAV of the animals that were in a slightly negative sodium balance was not correlated to renal sodium excretion. It is concluded that, in conscious rats, the increase in UDAV in response to feeding 1) depends on the supply of catecholamine precursors solely, 2) is dose dependent and saturable, and 3) is not affected by experimental diabetes mellitus.