The Effects of Bumetanide and Furosemide on Lung Liquid Secretion in Fetal Sheep

Cassin, S.; Gause, G.; Perks, A. M.

doi:10.3181/00379727-181-42276

Cited by 49 publications

(16 citation statements)

References 6 publications

(7 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In sheep, the flow rate of secreted tracheal liquid is ‫ف‬ 5 ml/h/ kg body wt at term (45,46). The fluid secretion is driven by active chloride transport across the lumenal membrane (45,47,48). Fluid secretion and maintenance of its specific composition may be important for lung morphogenesis (49)(50)(51).…”

Section: Discussionmentioning

confidence: 99%

Developmental changes in water permeability across the alveolar barrier in perinatal rabbit lung.

Carter

Umenishi²,

Matthay³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

Lung fluid is reabsorbed rapidly at birth to permit alveolar respiration. We reported previously that expression of aquaporins (AQP) 1, 4, and 5 in rat lung increased just after birth. The hypothesis was tested that the increased AQP expression is associated with increased osmotic water permeability (P f ) between the airspace and capillary compartments. P f was measured in isolated perfused fetal and newborn rabbit lungs using a pleural surface fluorescence method (

show abstract

Section: Discussionmentioning

confidence: 99%

Developmental changes in water permeability across the alveolar barrier in perinatal rabbit lung.

Carter

Umenishi²,

Matthay³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…The bumetanide-sensitive Na + /K + /2Cl − cotransporter has been shown to contribute to the Cl − secretion (Cassin, Gause & Perks, 1986), while the amiloridesensitive ion transport has been shown to play an important role in alveolar fluid absorption to permit future gas exchange during labor and immediately following birth (O'Brodovich, 1991(O'Brodovich, , 1996.…”

Section: Introductionmentioning

confidence: 99%

Roles of Ca 2+ and Protein Tyrosine Kinase in Insulin Action on Cell Volume via Na + and K + Channels and Na + /K + /2Cl − Cotransporter in Fetal Rat Alveolar Type II Pneumocyte

Marunaka

Niisato

O’Brodovich

et al. 1999

Journal of Membrane Biology

View full text Add to dashboard Cite

The aim of the present study was to investigate the roles of Ca2+ and protein tyrosine kinase (PTK) in the insulin action on cell volume in fetal rat (20-day gestational age) type II pneumocytes. Insulin (100 nm) increased cell volume in the presence of extracellular Ca2+ (1 mm), while cell shrinkage was induced by insulin in the absence of extracellular Ca2+ (<1 nm). This insulin action in a Ca2+-containing solution was completely blocked by co-application of bumetanide (50 microm, an inhibitor of Na+/K+/2Cl- cotransporter) and amiloride (10 microm, an inhibitor of epithelial Na+ channel), but not by the individual application of either bumetanide or amiloride. On the other hand, the insulin action on cell volume in a Ca2+-free solution was completely blocked by quinine (1 mm, a blocker of Ca2+-activated K+ channel), but not by bumetanide and/or amiloride. These observations suggest that insulin activates an amiloride-sensitive Na+ channel and a bumetanide-sensitive Na+/K+/2Cl- cotransporter in the presence of 1 mm extracellular Ca2+, that the stimulatory action of insulin on an amiloride-sensitive Na+ channel and a bumetanide-sensitive Na+/K+/2Cl- cotransporter requires Ca2+, and that in a Ca2+-free solution insulin activates a quinine-sensitive K+ channel but not in the presence of 1 mm Ca2+. The insulin action on cell volume in a Ca2+-free solution was almost completely blocked by treatment with BAPTA (10 microm) or thapsigargin (1 microM, an inhibitor of Ca2+-ATPase which depletes the intracellular Ca2+ pool). Further, lavendustin A (10 microm, an inhibitor of receptor type PTK) blocked the insulin action in a Ca2+-free solution. These observations suggest that the stimulatory action of insulin on a quinine-sensitive K+ channel is mediated through PTK activity in a cytosolic Ca2+-dependent manner. Lavendustin A, further, completely blocked the activity of the Na+/K+/2Cl- cotransporter in a Ca2+-free solution, but only partially blocked the activity of the Na+/K+/2Cl- cotransporter in the presence of 1 mm Ca2+. This observation suggests that the activity of the Na+/K+/2Cl- cotransporter is maintained through two different pathways; one is a PTK-dependent, Ca2+-independent pathway and the other is a PTK-independent, Ca2+-dependent pathway. Further, we observed that removal of extracellular Ca2+ caused cell shrinkage by diminishing the activity of the amiloride-sensitive Na+ channel and the bumetanide-sensitive Na+/K+/2Cl- cotransporter, and that removal of extracellular Ca2+ abolished the activity of the quinine-sensitive K+ channel. We conclude that the cell shrinkage induced by removal of extracellular Ca2+ results from diverse effects on the cotransporter and Na+ and K+ channels.

show abstract

“…In fetal sheep and guinea-pig lung, addition of the loop diuretic bumetanide or furosemide (specific NKCC inhibitors) to fetal lung liquid caused slowing of lung-liquid secretion or liquid absorption (13,14). Likewise, loop diuretics inhibited liquid secretion by distal lung explants from fetal rat lung (3,15) and decreased basal short-circuit current by excised fetal canine or rabbit trachea (16,17).…”

mentioning

confidence: 99%

Liquid and Ion Transport by Fetal Airway and Lung Epithelia of Mice Deficient in Sodium-Potassium-2-Chloride Transporter

Gillie

Pace

Coakley

et al. 2001

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Chloride (Cl(-)) movement across fetal lung epithelia is thought to be mediated by the sodium-potassium-2-Cl(-) cotransporter NKCC1. We studied the role of NKCC1 in Cl(-) and liquid secretion in late-gestation NKCC-null (-/-) and littermate control fetal mouse lung. NKCC -/- mice had decreased lung water compared with littermate controls (wet/dry: control, 8.01 +/- 0.09; NKCC -/-, 7.06 +/- 0.14). Liquid secretion by 17-d NKCC -/- distal lung explants was similar to control explants. Bumetanide inhibited basal liquid secretion in control but not NKCC -/- explants (expansion over 48 h: control, 35 +/- 4%; NKCC -/- 46 +/- 7%). Treatment with 4,4'-diisothiocyanto-stilbene-2,2'-disulfonic acid (DIDS) decreased liquid secretion in both control and NKCC -/- explants. Basal transepithelial potential difference (PD) of control tracheal explants was higher than that of NKCC -/- (control, -13.7 +/- 0.5 mV; NKCC -/-, -11.6 +/- 0.6 mV). Amiloride (10(-)(4) M) inhibited basal PD to the same extent in control and NKCC -/- mice. Terbutaline-stimulated hyperpolarization was less in NKCC -/- than in control tracheas (DeltaPD: control, -10.8 +/- 1.33 mV; NKCC -/-, -6.1 +/- 0.7 mV) and was inhibited by DIDS and acetazolamide in NKCC -/- but not wild-type explants. We conclude that NKCC is rate-limiting for transcellular Cl(-) transport, and that alternative anion transport mechanisms can sustain liquid production at near-normal levels in the fetal NKCC -/- mouse lung.

show abstract

The Effects of Bumetanide and Furosemide on Lung Liquid Secretion in Fetal Sheep

Cited by 49 publications

References 6 publications

Developmental changes in water permeability across the alveolar barrier in perinatal rabbit lung.

Developmental changes in water permeability across the alveolar barrier in perinatal rabbit lung.

Roles of Ca 2+ and Protein Tyrosine Kinase in Insulin Action on Cell Volume via Na + and K + Channels and Na + /K + /2Cl − Cotransporter in Fetal Rat Alveolar Type II Pneumocyte

Liquid and Ion Transport by Fetal Airway and Lung Epithelia of Mice Deficient in Sodium-Potassium-2-Chloride Transporter

Contact Info

Product

Resources

About