April 1, 2002AJP Lung Cellular and Molecular Physiology

β-Adrenergic regulation of amiloride-sensitive lung sodium channels

View Full Paper

Ask AI

Bookmark

Population

Alveolar type II (ATII) cells

Design

Preclinical

Authors

XCXijuan ChenShenyang Ligong University DEDouglas C. EatonElectrophysiology LJLucky JainMemorial Hermann

Discussion

Member takes

Implication

May enhance lung sodium transport in animal models; leaves open translation to human pulmonary edema therapies.

Structured PICO

Population

Alveolar type II (ATII) cells

Intervention

Exposure to cAMP, beta-adrenergic agonists (terbutaline, isoproterenol), forskolin, or cAMP analogs

Outcome

Activity of amiloride-sensitive cation channels (nonselective cation channel [NSC] and highly selective channel [HSC])surrogate

Beta-adrenergic stimulation increases lung sodium transport via PKA activation, which increases HSC number and intracellular calcium to increase NSC open probability.

Cite This Study

Chen et al. (2002) studied this question.

synapsesocial.com/papers/6a7d32cbe9ec6b5ffa6e4714 https://doi.org/10.1152/ajplung.00356.2001

View Full Paper

Ask AI

Bookmark

β-Adrenergic regulation of amiloride-sensitive lung sodium channels

Discussion

Member takes

Implication

Structured PICO

Cite This Study

β-Adrenergic regulation of amiloride-sensitive lung sodium channels

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider