• Media type: E-Article
  • Title: cAMP-induced changes of apical membrane potentials of confluent H441 monolayers
  • Contributor: Lazrak, Ahmed; Matalon, Sadis
  • Published: American Physiological Society, 2003
  • Published in: American Journal of Physiology-Lung Cellular and Molecular Physiology, 285 (2003) 2, Seite L443-L450
  • Language: English
  • DOI: 10.1152/ajplung.00412.2002
  • ISSN: 1040-0605; 1522-1504
  • Origination:
  • Footnote:
  • Description: We recorded apical membrane potentials ( Va) of H441 cells [a human lung cell line exhibiting both epithelial Na+ (ENaC) and CFTR-type channels] grown as confluent monolayers, using the microelectrode technique in current-clamp mode before, during, and after perfusion of the apical membranes with 10 μM forskolin. When perfused with normal Ringer solution, the cells had a Va of -43 ± 10 mV (means ± SD; n = 31). Perfusion with forskolin resulted in sustained depolarization by 25.0 ± 3.5 mV (means ± SD; n = 23) and increased the number, open time, and the open probability of a 4.2-pS ENaC. In contrast to a previous report (Jiang J, Song C, Koller BH, Matthay MA, and Verkman AS. Am J Physiol Cell Physiol 275: C1610–C1620, 1998), no transient hyperpolarization was observed. The forskolin-induced depolarization of Va was almost totally prevented by pretreatment of monolayers with 10 μM amiloride or by substitution of Na+ ions in the bath solution with N-methyl-d-glucamine. These findings indicate that cAMP stimulation of Na+ influx across H441 confluent monolayers results from activation of an amiloride-sensitive apical Na+ conductance and not from Va hyperpolarization due to Cl- influx through CFTR-type channels.
  • Access State: Open Access