Benzimidazolones enhance the function of epithelial Na⁺ transport

Br J Pharmacol. 2013 Mar;168(6):1329-40. doi: 10.1111/bph.12027.

Abstract

Background and purpose: Pharmacological enhancement of vectorial Na⁺ transport may be useful to increase alveolar fluid clearance. Herein, we investigated the influence of the benzimidazolones 1-ethyl-1,3-dihydro-2-benzimidazolone (1-EBIO), 5,6-dichloro-1-EBIO (DC-EBIO) and chlorzoxazone on vectorial epithelial Na⁺ transport.

Experimental approach: Effects on vectorial Na⁺ transport and amiloride-sensitive apical membrane Na⁺ permeability were determined by measuring short-circuit currents (I(SC)) in rat fetal distal lung epithelial (FDLE) monolayers. Furthermore, amiloride-sensitive membrane conductance and the open probability of epithelial Na⁺ channels (ENaC) were determined by patch clamp experiments using A549 cells.

Key results: I(SC) was increased by approximately 50% after addition of 1-EBIO, DC-EBIO and chlorzoxazone. With permeabilized basolateral membranes in the presence of a 145:5 apical to basolateral Na⁺ gradient, the benzimidazolones markedly increased amiloride-sensitive I(SC). 5-(N-Ethyl-N-isopropyl)amiloride-induced inhibition of I(SC) was not affected. The benzamil-sensitive I(SC) was increased in benzimidazolone-stimulated monolayers. Pretreating the apical membrane with amiloride, which inhibits ENaC, completely prevented the stimulating effects of benzimidazolones on I(SC). Furthermore, 1-EBIO (1 mM) and DC-EBIO (0.1 mM) significantly increased (threefold) the open probability of ENaC without influencing current amplitude. Whole cell measurements showed that DC-EBIO (0.1 mM) induced an amiloride-sensitive increase in membrane conductance.

Conclusion and implications: Benzimidazolones have a stimulating effect on vectorial Na⁺ transport. The antagonist sensitivity of this effect suggests the benzimidazolones elicit this action by activating the highly selective ENaC currents. Thus, the results demonstrate a possible new strategy for directly enhancing epithelial Na⁺ transport.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Benzimidazoles / antagonists & inhibitors
  • Benzimidazoles / pharmacology*
  • Cell Line
  • Cell Membrane Permeability / drug effects
  • Cell Polarity / drug effects
  • Cells, Cultured
  • Chlorzoxazone / antagonists & inhibitors
  • Chlorzoxazone / pharmacology*
  • Epithelial Sodium Channel Agonists / antagonists & inhibitors
  • Epithelial Sodium Channel Agonists / pharmacology*
  • Epithelial Sodium Channel Blockers / pharmacology
  • Epithelial Sodium Channels / metabolism*
  • Fetus / cytology
  • Humans
  • Membrane Potentials / drug effects
  • Patch-Clamp Techniques
  • Pulmonary Alveoli / cytology
  • Pulmonary Alveoli / drug effects*
  • Pulmonary Alveoli / metabolism
  • Rats
  • Respiratory Mucosa / cytology
  • Respiratory Mucosa / drug effects*
  • Respiratory Mucosa / metabolism
  • Single-Cell Analysis
  • Sodium / metabolism

Substances

  • 5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one
  • Benzimidazoles
  • Epithelial Sodium Channel Agonists
  • Epithelial Sodium Channel Blockers
  • Epithelial Sodium Channels
  • Sodium
  • Chlorzoxazone
  • 1-ethyl-2-benzimidazolinone