Trimethoprim inhibits renal H+-K+-ATPase in states of K+ depletion
Copyright policy )Trimethoprim inhibits renal H+-K+-ATPase in states of K+ depletion
The antibiotic trimethoprim (TMP) often mediates K+ retention and metabolic acidosis. We suggest a revision of the underlying mechanism that causes metabolic acidosis. Our results indicate that TMP-induced metabolic acidosis is secondary to epithelial Na+ channel-dependent K+ retention. Under control dietary conditions, TMP does not per se inhibit collecting duct H+ secretion. These findings add further argument against a physiologically relevant voltage-dependent mechanism of collecting duct H+ excretion.
- University Medical Centre Mannheim Germany
- Aarhus University Denmark
- Heidelberg University Germany
metabolic acidosis, Epithelial Sodium Channels/metabolism, Trimethoprim/pharmacology, Swine, Sodium, sulfamethoxazole, H(+)-K(+)-Exchanging ATPase/metabolism, Trimethoprim, Anti-Bacterial Agents/pharmacology, Anti-Bacterial Agents, Mice, H(+)-K(+)-Exchanging ATPase, Sodium/metabolism, benzamil, Acidosis/metabolism, Animals, Kidney Tubules, Collecting, Epithelial Sodium Channels, Acidosis, Kidney Tubules, Collecting/metabolism, epithelial Na+ channel
metabolic acidosis, Epithelial Sodium Channels/metabolism, Trimethoprim/pharmacology, Swine, Sodium, sulfamethoxazole, H(+)-K(+)-Exchanging ATPase/metabolism, Trimethoprim, Anti-Bacterial Agents/pharmacology, Anti-Bacterial Agents, Mice, H(+)-K(+)-Exchanging ATPase, Sodium/metabolism, benzamil, Acidosis/metabolism, Animals, Kidney Tubules, Collecting, Epithelial Sodium Channels, Acidosis, Kidney Tubules, Collecting/metabolism, epithelial Na+ channel
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