Tumor necrosis factor induces sodium retention in diabetic rats through sequential effects on distal tubule cells.

摘要: Tumor necrosis factor induces sodium retention in diabetic rats through sequential effects on distal tubule cells. Background (TNF) contributes to during diabetes. TNF selectively stimulates uptake cells isolated from rats, but not control rats. We propose that are sensitized acute of Methods examined TNF-stimulated chronically cultured with exogenous and freshly treated a specific inhibitor. also tested the transport intracellular signaling pathway underlying TNF-induced pharmacologic inhibitors. Results Chronic exposure vitro time- dose-dependent manner, inhibition vivo diabetes prevented sensitization. receptor expression was equivalent both In cells, blocked by amiloride PD098059, inhibitors epithelial channels extracellular signal-related protein kinase (ERK) activation, respectively. Conclusion alters consecutive chronic effects. leads sensitization permits activation channel (ENaC). These findings consistent mechanism which actions at cellular level contribute whole animal