Opposite effects of ANP receptors in attenuation of LPS-induced endothelial permeability and lung injury.
MouseEndotoxin/LPSC57BL/6MaleAdministered in vivo and applied to endothelial cell cultures in vitro
Model: Lipopolysaccharide-induced acute lung injury in mice and lipopolysaccharide-induced barrier disruption in human pulmonary endothelial cells
Lipopolysaccharide increased ANP and NPR-A expression; NPR-A inhibition augmented endothelial permeability and exacerbated lung injury in vivo, whereas NPR-C inhibition attenuated barrier disruption and reduced bronchoalveolar lavage cell count and protein content.
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