Endothelin decreases lung edema clearance and Na,K‐ATPase activity in alveolar epithelial cells via ET‐B receptor and Nitric Oxide generation

Comellas, A.P.; Litvan, Juan; Briva, Arturo; Lecuona, Emilia; Chen, Jiwang; Sznajder, Jacob I.

doi:10.1096/fasebj.20.5.a1071-c

FASEB j.

2006

DOI: 10.1096/fasebj.20.5.a1071-c

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Endothelin decreases lung edema clearance and Na,K‐ATPase activity in alveolar epithelial cells via ET‐B receptor and Nitric Oxide generation

A.P. Comellas

Juan Litvan

Arturo Briva

et al.

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2009

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Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ET_B Receptor

Comellas¹,

Briva²,

Dada³

et al. 2009

Am J Respir Crit Care Med

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Rationale: Endothelin-1 (ET-1) is increased in patients with highaltitude pulmonary edema and acute respiratory distress syndrome, and these patients have decreased alveolar fluid reabsorption (AFR). Objectives: To determine whether ET-1 impairs AFR via activation of endothelial cells and nitric oxide (NO) generation. Methods: Isolated perfused rat lung, transgenic rats deficient in ET B receptors, coincubation of lung human microvascular endothelial cells (HMVEC-L) with rat alveolar epithelial type II cells or A549 cells, ouabain-sensitive 86 Rb 1 uptake. Measurements and Main Results: The ET-1-induced decrease in AFR was prevented by blocking the endothelin receptor ET B , but not ET A . Endothelial-epithelial cell interaction is required, as direct exposure of alveolar epithelial cells (AECs) to ET-1 did not affect Na,K-ATPase function or protein abundance at the plasma membrane, whereas coincubation of HMVEC-L and AECs with ET-1 decreased Na,K-ATPase activity and protein abundance at the plasma membrane. Exposing transgenic rats deficient in ET B receptors in the pulmonary vasculature (ET-B 2/2 ) to ET-1 did not decrease AFR or Na,K-ATPase protein abundance at the plasma membrane of AECs. Exposing HMVEC-L to ET-1 led to increased NO, and the ET-1-induced down-regulation of Na,K-ATPase was prevented by the NO synthase inhibitor L-NAME, but not by a guanylate cyclase inhibitor. Conclusions: We provide the first evidence that ET-1, via an endothelial-epithelial interaction, leads to decreased AFR by a mechanism involving activation of endothelial ET B receptors and NO generation leading to alveolar epithelial Na,K-ATPase down-regulation in a cGMP-independent manner.

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Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ET_B Receptor

Comellas¹,

Briva²,

Dada³

et al. 2009

Am J Respir Crit Care Med

Self Cite

View full text Add to dashboard Cite

show abstract

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Endothelin decreases lung edema clearance and Na,K‐ATPase activity in alveolar epithelial cells via ET‐B receptor and Nitric Oxide generation

Cited by 1 publication

References 0 publications

Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ET_B Receptor

Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ET_B Receptor

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Endothelin decreases lung edema clearance and Na,K‐ATPase activity in alveolar epithelial cells via ET‐B receptor and Nitric Oxide generation

Cited by 1 publication

References 0 publications

Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ETB Receptor

Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ETB Receptor

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About

Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ET_B Receptor

Endothelin-1 Impairs Alveolar Epithelial Function via Endothelial ET_B Receptor