Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 285, Issue 2, Pages L443-L450Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00412.2002
Keywords
forskolin; epithelial sodium channel; cystic fibrosis transmembrane; conductance regulator; current clamp; patch clamp; single channel currents; amiloride; glibenclamide
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Funding
- NHLBI NIH HHS [HL-31197, HL-51173] Funding Source: Medline
- NIDDK NIH HHS [P30 DK-54781] Funding Source: Medline
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We recorded apical membrane potentials (V-a) 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 muM forskolin. When perfused with normal Ringer solution, the cells had a V-a 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 V-a was almost totally prevented by pretreatment of monolayers with 10 muM 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 V-a hyperpolarization due to Cl- influx through CFTR-type channels.
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