<i>Background:</i> The occurrence of complementary functions in sodium transport between the intestine and the kidney was suggested to occur when the renal function is immature or compromised and jejunal dopamine has been implicated in this renal-intestinal cross-talk. The jejunal sodium transport was not previously evaluated in the nephrotic syndrome. <i>Methods:</i> We examined the jejunal Na⁺,K⁺-ATPase activity and the role of dopamine in puromycin aminonucleoside (PAN) and HgCl₂-induced nephrotic syndrome rat models. <i>Results:</i> In both nephrotic syndrome rat models, the jejunal Na⁺,K⁺-ATPase activity was reduced during greatest sodium retention and ascites accumulation (PAN nephrosis, day 7; HgCl₂ nephrosis, day 14), whereas during enhanced sodium excretion and ascites mobilization the jejunal Na⁺,K⁺-ATPase activity was increased in HgCl₂ nephrosis (day 21) and was similar to controls in PAN nephrosis (day 14). In both PAN- and HgCl₂-induced nephrosis, the jejunal aromatic <i>L</i>-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of jejunal dopamine, did not differ from controls. In addition, the jejunal Na⁺,K⁺-ATPase activity was not sensitive to inhibition by dopamine (1 µ<i>M</i>) in both experimental groups throughout the study. <i>Conclusions:</i> In the nephrotic syndrome the jejunal Na⁺,K⁺-ATPase activity may respond in a compensatory way to changes in extracellular volume, through dopamine-independent mechanisms.