β-Adrenoceptor-mediated control of apical membrane conductive properties in fetal distal lung epithelia

TY - JOUR

T1 - β-Adrenoceptor-mediated control of apical membrane conductive properties in fetal distal lung epithelia

AU - Collett, A.

AU - Ramminger, S. J.

AU - Olver, R. E.

AU - Wilson, S. M.

N1 - dc.publisher: American Physiological Society 10.1152/ajplung.00142.2001-invalid DOI. Senior author responsible for strategy, funding, planning, analysis and writing paper demonstrating that Irrespective of their hormonal status, fetal distal lung epithelial cells express beta-adrenoceptors that are functionally coupled to adenylate cyclase and allow agonists to modulate anion conductance.

PY - 2002

Y1 - 2002

N2 - Distal lung epithelial cells isolated from fetal rats were cultured (48 h) on permeable supports so that transepithelial ion transport could be quantified electrometrically. Unstimulated cells generated a short-circuit current (I sc) that was inhibited (~80%) by apical amiloride. The current is thus due, predominantly, to the absorption of Na+ from the apical solution. Isoprenaline increased the amiloride-sensitive I sc about twofold. Experiments in which apical membrane Na+ currents were monitored in basolaterally permeabilized cells showed that this was accompanied by a rise in apical Na+ conductance (G Na+). Isoprenaline also increased apical Cl- conductance (G Cl-) by activating an anion channel species sensitive to glibenclamide but unaffected by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). The isoprenaline-evoked changes inG Na+ and G Cl-could account for the changes in I sc observed in intact cells. Glibenclamide had no effect upon the isoprenaline-evoked stimulation of I sc orG Na+ demonstrating that the rise inG Cl- is not essential to the stimulation of Na+ transport.

AB - Distal lung epithelial cells isolated from fetal rats were cultured (48 h) on permeable supports so that transepithelial ion transport could be quantified electrometrically. Unstimulated cells generated a short-circuit current (I sc) that was inhibited (~80%) by apical amiloride. The current is thus due, predominantly, to the absorption of Na+ from the apical solution. Isoprenaline increased the amiloride-sensitive I sc about twofold. Experiments in which apical membrane Na+ currents were monitored in basolaterally permeabilized cells showed that this was accompanied by a rise in apical Na+ conductance (G Na+). Isoprenaline also increased apical Cl- conductance (G Cl-) by activating an anion channel species sensitive to glibenclamide but unaffected by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). The isoprenaline-evoked changes inG Na+ and G Cl-could account for the changes in I sc observed in intact cells. Glibenclamide had no effect upon the isoprenaline-evoked stimulation of I sc orG Na+ demonstrating that the rise inG Cl- is not essential to the stimulation of Na+ transport.

KW - Alveolar ion transport

KW - Ussing chambers

KW - Permeabilized epithelia

U2 - 10.?1152/?ajplung.?00142.?2001

DO - 10.?1152/?ajplung.?00142.?2001

M3 - Article

SN - 1040-0605

VL - 282

SP - 621

EP - 630

JO - American Journal of Physiology: Lung Cellular and Molecular Physiology

JF - American Journal of Physiology: Lung Cellular and Molecular Physiology

IS - 4

ER -