Mechanical Forces Impair Alveolar Ion Transport Processes – A Putative Mechanism Contributing to the Formation of Pulmonary Edema

Fronius, Martin

doi:10.5772/26036

Cited by 1 publication

(2 citation statements)

References 84 publications

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“…The alveolar epithelium is not only the site of gas exchange but is also the area most affected by the mechanical strain (5, 41) caused by positive and negative pressures during respiration (41). In normal breathing movements, transpulmonary pressures up to 30 cmH 2 O can exert strain and subsequent changes in the length of the surface of ~4% during normal breathing and up to 25% during deep inspirations (50).…”

Section: Discussionmentioning

confidence: 99%

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Hydrostatic pressure activates ATP‐sensitive K⁺channels in lung epithelium by ATP release through pannexin and connexin hemichannels

Richter

Kiefer

Grzesik³

et al. 2013

FASEB j.

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Lungs of air-breathing vertebrates are constantly exposed to mechanical forces and therefore are suitable for investigation of mechanotransduction processes in nonexcitable cells and tissues. Freshly dissected Xenopus laevis lungs were used for transepithelial short-circuit current (ISC) recordings and were exposed to increased hydrostatic pressure (HP; 5 cm fluid column, modified Ussing chamber). I(SC) values obtained under HP (I(5cm)) were normalized to values before HP (I(0cm)) application (I(5cm)/I(0cm)). Under control conditions, HP decreased I(SC) (I(5cm)/I(0cm)=0.84; n=68; P<0.0001). This effect was reversible and repeatable ≥30 times. Preincubation with ATP-sensitive K(+) channel (K(ATP)) inhibitors (HMR1098 and glibenclamide) prevented the decrease in I(SC) (I(5cm)/I(0cm): HMR1098=1.19, P<0.0001; glibenclamide=1.11, P<0.0001). Similar effects were observed with hemichannel inhibitors (I(5cm)/I(0cm): meclofenamic acid=1.09, P<0.0001; probenecid=1.0, P<0.0001). The HP effect was accompanied by release of ATP (P<0.05), determined by luciferin-luciferase luminescence in perfusion solution from the luminal side of an Ussing chamber. ATP release was abrogated by both meclofenamic acid and probenecid. RT-PCR experiments revealed the expression of pannexin and connexin hemichannels and KATP subunit transcripts in X. laevis lung. These data show an activation of KATP in pulmonary epithelial cells in response to HP that is induced by ATP release through mechanosensitive pannexin and connexin hemichannels. These findings represent a novel mechanism of mechanotransduction in nonexcitable cells.

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Section: Discussionmentioning

confidence: 99%

“…From lungfishes to mammals, the morphology of the air–blood barrier is highly conserved (39). Its structure is referred to as a “3‐ply” design represented by the pulmonary epithelium, the basal lamina, and the endothelium (40, 41). Further, the apical side of epithelial cells is entirely covered by a thin fluid layer (42).…”

Section: Discussionmentioning

confidence: 99%

Hydrostatic pressure activates ATP‐sensitive K⁺channels in lung epithelium by ATP release through pannexin and connexin hemichannels

Richter

Kiefer

Grzesik³

et al. 2013

FASEB j.

Self Cite

View full text Add to dashboard Cite

show abstract

Mechanical Forces Impair Alveolar Ion Transport Processes – A Putative Mechanism Contributing to the Formation of Pulmonary Edema

Cited by 1 publication

References 84 publications

Hydrostatic pressure activates ATP‐sensitive K⁺channels in lung epithelium by ATP release through pannexin and connexin hemichannels

Hydrostatic pressure activates ATP‐sensitive K⁺channels in lung epithelium by ATP release through pannexin and connexin hemichannels

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Mechanical Forces Impair Alveolar Ion Transport Processes – A Putative Mechanism Contributing to the Formation of Pulmonary Edema

Cited by 1 publication

References 84 publications

Hydrostatic pressure activates ATP‐sensitive K+channels in lung epithelium by ATP release through pannexin and connexin hemichannels

Hydrostatic pressure activates ATP‐sensitive K+channels in lung epithelium by ATP release through pannexin and connexin hemichannels

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Hydrostatic pressure activates ATP‐sensitive K⁺channels in lung epithelium by ATP release through pannexin and connexin hemichannels

Hydrostatic pressure activates ATP‐sensitive K⁺channels in lung epithelium by ATP release through pannexin and connexin hemichannels