PROTEIN-INDUCED INCREASE IN URINARY DOPAMINE IN NORMAL AND DIABETIC RATS - ROLE OF CATECHOLAMINE PRECURSORS

Feeding and protein intake increase renal dopamine excretion (UDAV), H ere the contribution of amino acids (AA), L-tyrosine (Tyr), and L-phen ylalanine (Phe) to UDAV in conscious normal rats and in animals with s treptozotocin (STZ)-induced (60 mg/kg) diabetes mellitus was investiga ted Feeding a standard chow (17.3% protein) increased UDAV in normal r ats over twofold compared with the fasted state, but the effect was co mpletely abolished by feeding a low-protein (LP, 0.03%) diet. In STZ r ats, UDAV was equal to that of normal rats during the fasted periods b ut was higher in fed animals, resulting most likely from the higher pr otein intake of STZ rats. In another series, rats on LP diet were give n AA solutions (7, 14, and 21 g . kg(-1). 24 h(-1)) by gastric tube, w hich dose dependently increased UDAV to 67.3 +/- 4.3, 91.1 +/- 5.0, an d 129 +/- 17 nmol . kg(-1). day(-1), respectively, compared with tap w ater 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 (AA(PT)) increased UDAV twofold compared with H2O, whereas AA solution without Tyr and Phe did not change UDAV. Tyr or Phe alone inc reased UDAV to the saute extent as observed in AA(PT) Higher doses of Tyr further increased UDAV dose dependently but with saturation charac teristics. 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 dos e dependent and saturable, and 3) is not affected by experimental diab etes mellitus.