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Regional intestinal adaptations in Na + ,K + ‐ATPase in experimental colitis and the contrasting effects of interferon‐ γ

2005; Wiley; Volume: 183; Issue: 2 Linguagem: Inglês

10.1111/j.1365-201x.2004.01388.x

1365-201X

Fernando Magro, Sónia Fraga, Tiago Ribeiro, Patrı́cio Soares-da-Silva,

Potassium and Related Disorders

Abstract Aims: This study evaluated Na + ,K + ‐ATPase activity and the abundance of α 1 subunit Na + ,K + ‐ATPase in experimental colitis and gathered evidence on the effects of interferon‐ γ (IFN‐ γ ) on intestinal Na + ,K + ‐ATPase. Methods: Colitis was induced by the intrarectal administration of 2,4,6‐trinitrobenzene sulphonic acid (TNBS, 30 mg/250 μ L). Na + ,K + ‐ATPase activity was determined as the difference between total and ouabain‐insensitive ATPase. The abundance of Na + ,K + ‐ATPase was analysed by immunoblotting. Results: Na + ,K + ‐ATPase activity was markedly reduced in the proximal colonic mucosa of TNBS‐treated rats, whereas upstream in the terminal ileal mucosa a marked increase in sodium pump activity was observed. At the jejunal level no significant changes in Na + ,K + ‐ATPase activity were observed between TNBS‐treated rats and corresponding controls (ethanol‐treated rats). No changes were observed in the abundance of α 1 subunit Na + ,K + ‐ATPase in the proximal colon, terminal ileum and jejunum. The administration of IFN‐ γ (50 000 U) 48 h before sacrifice reduced both Na + ,K + ‐ATPase activity and the abundance of α 1 subunit Na + ,K + ‐ATPase in the proximal colon. Dexamethasone prevented colonic inflammation and decreases in proximal colonic Na + ,K + ‐ATPase activity in TNBS‐treated rats, but did not affect the INF‐ γ ‐induced decrease in colonic Na + ,K + ‐ATPase activity. Conclusions: The increase in ileal Na + ,K + ‐ATPase activity upstream to the lesioned colonic mucosa, where Na + ,K + ‐ATPase activity was markedly reduced, might indicate a compensatory process to counteract the decrease in water and electrolyte absorption at the colonic level. This decrease in colonic Na + ,K + ‐ATPase activity is likely not related to INF‐ γ ‐induced downregulation of Na + ,K + ‐ATPase.