Alveolar liquid clearance in lung injury: Evaluation of the impairment of the β2-adrenergic agonist response in an ischemia-reperfusion lung injury model

The objective of this study was to determine if downregulation of the β2-AR could explain the lack of response to β2-agonists in this lung injury model. In an in vivo canine model of lung transplantation, we observed no change in β2-AR concentration or affinity in the injured transplanted lungs compared to the native lungs. Furthermore, we could not enhance ALC in transplanted lungs with dcAMP + aminophylline, a treatment that bypasses the β2-adrenergic receptor and is known to stimulate ALC in normal lungs. However, transplantation decreased αENaC expression in the lungs by 50%. We conclude that the lack of response to β2-agonists in ischemia-reperfusion-induced lung injury is not associated with significant downregulation of the β2-adrenergic receptors but is attributable to decreased expression of the ENaC channel, which is essential for sodium transport and alveolar liquid clearance in the lung.
Source: Respiratory Physiology and Neurobiology - Category: Respiratory Medicine Source Type: research