Urinary dopamine excretion was studied in seven different groups of rats (n = 6-12) with the following treatment regimens: normal chow and tap water (controls, CON), single administration of furosemide 20 mg/kg i.p. on day 1 and subsequent feeding of low sodium chow (low salt, LS), normal chow and 1 % NaCl as drinking water (high salt HS) normal chow and 1% NaCl plus deoxycorticosterone acetate 1 mg/kg/day i.p. (high salt plus DOCA, HS+DOCA); carbidopa 20 mg/kg/day p.o. (CDP) was administered in animals on normal chow (CON+CDP), in high salt rats (HS+ CDP), andinratsonhighsaltplusDOCA(HS+DOCA+CDP).Onday5, rats were placed in metabolic cages with free access to their respective drinking solution; chow was withheld. Urine was collected for 24 h and analyzed for sodium, creatinine, and dopamine. Urinary dopamine excretion rates did not change in proportion to large differences in sodium excretion in LS, HS, and HS+DOCA animals compared to CON. Only when urinary dopamine excretion of HS rats was compared to the LS group there was a moderate but significant increase of 27%. In the groups treated with CDP renal dopamine excretion was decreased by approximately 60% in comparison to the groups with the respective treatment condition but without CDP. Urinary sodium output was unchanged by CDP in CON+ CDP animals compared to CON. In HS+CDP and HS+DOCA+CDP groups renal sodium excretion was reduced by half compared to the HS and HS+DOCA groups, respectively. However, this effect was accompanied by a similar, approximately 55% reduction of oral volume and sodium intake. Renal sodium excretory capacity was unchanged by CDP treatment. Daily sodium balance (intake minus output) was similar in all experimental groups. We conclude that (1) changes in urinary sodium output during CDP treatment could be caused by extrarenal factors, and (2) sodium balance should be controlled in experiments on renal dopamine production in conscious animals. The results do not support the concept that endogenous dopamine is a crucial factor in the renal response to oral sodium load in conscious rats.