Chronic Ethanol Exposure Stimulates Endothelial Cell Nitric Oxide Production through PI-3 Kinase-and hsp90-dependent Mechanisms

Abstract

These results indicate that chronic EtOH exposure increases endothelial NO production by increasing eNOS protein levels through PI3 K-dependent up regulation of eNOS gene transcription and by increasing interactions between eNOS and hsp90. These findings clarify mechanisms by which chronic EtOH stimulation modulates vascular endothelial function and suggest new targets for investigation and intervention in EtOH-induced alterations in susceptibility to lung injury.