Alpha 1-adrenergic stimulation differentially regulates ether-linked diacylglycerols in airway epithelial cells from normal and cystic fibrosis patients.

Alpha 1-adrenergic stimulation of human airway epithelial cells induces a transient increase in polyphosphoinositide turnover coincident with augmented Na+Cl-(K+) cotransport activity. This activation of airway epithelial cells also results in a biphasic elevation of diacylglycerols. To better understand the significance of these distinct diacylglycerol pools, we now characterize the mass of ether- and ester-linked diacylglycerol species. We demonstrate that the relative mass of ether-linked diacylglycerols is reduced in airway epithelium from cystic fibrosis patients in the presence or absence of alpha 1-adrenergic stimulation. This reduction in ether-linked diacylglycerol mass may represent a compensatory mechanism to help maintain normal chloride influx in cystic fibrosis patients.