Jejunal dopamine and Na+,K+-ATPase activity in nephrotic syndrome

• Autor(a) principal: Maria Maia
• Data de Publicação: 2005
• Outros Autores: Mónica Rodrigues, Paula Serrão, Manuel Pestana
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: https://hdl.handle.net/10216/1906
• topic: Ciências da Saúde; Health sciences

Background: 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. Methods: We examined the jejunal Na+,K+-ATPase activity and the role of dopamine in puromycin aminonucleoside (PAN) and HgCl2-induced nephrotic syndrome rat models. Results: 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 IHgCl2 nephrosis (day 21) land was similar to controls in PAN nephrosis (day 14). In both PAN- and HgCl2-induced nephrosis, the jejunal aromatic L-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 mu M) in both experimental groups throughout the study. Conclusions: 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. Copyright (C) 2005 S, Karger AG, Basel.