Sodium transport and intracellular sodium activity in cultured human nasal epithelium

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Sodium transport and intracellular sodium activity in cultured human nasal epithelium. / Willumsen, Niels J.; Boucher, Richard C.

I: American Journal of Physiology: Cell Physiology, Bind 261, Nr. 2, 1991, s. C319-C331.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Willumsen, NJ & Boucher, RC 1991, 'Sodium transport and intracellular sodium activity in cultured human nasal epithelium', American Journal of Physiology: Cell Physiology, bind 261, nr. 2, s. C319-C331. <http://ajpcell.physiology.org/cgi/content/abstract/261/2/C319>

APA

Willumsen, N. J., & Boucher, R. C. (1991). Sodium transport and intracellular sodium activity in cultured human nasal epithelium. American Journal of Physiology: Cell Physiology, 261(2), C319-C331. http://ajpcell.physiology.org/cgi/content/abstract/261/2/C319

Vancouver

Willumsen NJ, Boucher RC. Sodium transport and intracellular sodium activity in cultured human nasal epithelium. American Journal of Physiology: Cell Physiology. 1991;261(2):C319-C331.

Author

Willumsen, Niels J. ; Boucher, Richard C. / Sodium transport and intracellular sodium activity in cultured human nasal epithelium. I: American Journal of Physiology: Cell Physiology. 1991 ; Bind 261, Nr. 2. s. C319-C331.

Bibtex

@article{1826bb6074d111dbbee902004c4f4f50,
title = "Sodium transport and intracellular sodium activity in cultured human nasal epithelium",
abstract = "Human airway epithelia are predominantly Na(+)-absorbing epithelia. To investigate the mechanisms for Na+ absorption across airway epithelia, the driving forces and paths for Na+ translocation across each membrane wereexamined with double-barreled Na(+)-selective microelectrodes in cultured human nasal epithelium (HNE). Under control conditions, intracellular Na+ activity (acNa) was 23 +/- 1 mM (n = 44 preparations, 393 impalements).Amiloride (10(-4) M) hyperpolarized the apical membrane and increased the fractional apical membrane resistance but did not affect acNa. Exposure to Na(+)-free luminal solution induced bioelectric responses similar to amiloride but also reduced acNa to 8 +/- 1 mM. Reduction of luminal Na+ concentration ([Na+]) in the presence of amiloride also reduced acNa without further changes in bioelectric parameters. Reduction of serosal [Na+] decreased aNac, a response blocked by bumetanide (10(-4) M). Ouabain (10(-4) M, serosal) led to a reduction in equivalent short-circuit current (Ieq) and increase in acNa. We conclude that 1) acNa is higher in HNE than in most mammalian epithelial cells, 2) the apical membrane expresses a conductive Na+ path, and 3) the basolateral membrane transports Na+ via the Na(+)-K(+)-adenosinetriphosphatase and a Na(+)-K(+)-2Cl- cotransport system.",
author = "Willumsen, {Niels J.} and Boucher, {Richard C.}",
year = "1991",
language = "English",
volume = "261",
pages = "C319--C331",
journal = "American Journal of Physiology: Cell Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "2",

}

RIS

TY - JOUR

T1 - Sodium transport and intracellular sodium activity in cultured human nasal epithelium

AU - Willumsen, Niels J.

AU - Boucher, Richard C.

PY - 1991

Y1 - 1991

N2 - Human airway epithelia are predominantly Na(+)-absorbing epithelia. To investigate the mechanisms for Na+ absorption across airway epithelia, the driving forces and paths for Na+ translocation across each membrane wereexamined with double-barreled Na(+)-selective microelectrodes in cultured human nasal epithelium (HNE). Under control conditions, intracellular Na+ activity (acNa) was 23 +/- 1 mM (n = 44 preparations, 393 impalements).Amiloride (10(-4) M) hyperpolarized the apical membrane and increased the fractional apical membrane resistance but did not affect acNa. Exposure to Na(+)-free luminal solution induced bioelectric responses similar to amiloride but also reduced acNa to 8 +/- 1 mM. Reduction of luminal Na+ concentration ([Na+]) in the presence of amiloride also reduced acNa without further changes in bioelectric parameters. Reduction of serosal [Na+] decreased aNac, a response blocked by bumetanide (10(-4) M). Ouabain (10(-4) M, serosal) led to a reduction in equivalent short-circuit current (Ieq) and increase in acNa. We conclude that 1) acNa is higher in HNE than in most mammalian epithelial cells, 2) the apical membrane expresses a conductive Na+ path, and 3) the basolateral membrane transports Na+ via the Na(+)-K(+)-adenosinetriphosphatase and a Na(+)-K(+)-2Cl- cotransport system.

AB - Human airway epithelia are predominantly Na(+)-absorbing epithelia. To investigate the mechanisms for Na+ absorption across airway epithelia, the driving forces and paths for Na+ translocation across each membrane wereexamined with double-barreled Na(+)-selective microelectrodes in cultured human nasal epithelium (HNE). Under control conditions, intracellular Na+ activity (acNa) was 23 +/- 1 mM (n = 44 preparations, 393 impalements).Amiloride (10(-4) M) hyperpolarized the apical membrane and increased the fractional apical membrane resistance but did not affect acNa. Exposure to Na(+)-free luminal solution induced bioelectric responses similar to amiloride but also reduced acNa to 8 +/- 1 mM. Reduction of luminal Na+ concentration ([Na+]) in the presence of amiloride also reduced acNa without further changes in bioelectric parameters. Reduction of serosal [Na+] decreased aNac, a response blocked by bumetanide (10(-4) M). Ouabain (10(-4) M, serosal) led to a reduction in equivalent short-circuit current (Ieq) and increase in acNa. We conclude that 1) acNa is higher in HNE than in most mammalian epithelial cells, 2) the apical membrane expresses a conductive Na+ path, and 3) the basolateral membrane transports Na+ via the Na(+)-K(+)-adenosinetriphosphatase and a Na(+)-K(+)-2Cl- cotransport system.

M3 - Journal article

VL - 261

SP - C319-C331

JO - American Journal of Physiology: Cell Physiology

JF - American Journal of Physiology: Cell Physiology

SN - 0363-6143

IS - 2

ER -

ID: 304831