AJP - Gastrointestinal and Liver Physiology, Vol 272, Issue 3 605-G611, Copyright © 1997 by American Physiological Society

ARTICLES

Endothelin-1 production by hepatic endothelial cells: characterization and augmentation by endotoxin exposure

A. T. Eakes, K. M. Howard, J. E. Miller and M. S. Olson
Department of Biochemistry, University of Texas Health Science Center at San Antonio, 78284-7760, USA.

Activation of endothelin (ET) receptors in the liver causes vasoconstriction, glucose production, and lipid and peptide mediator synthesis. In the intact rat, a bolus infusion of endotoxin into a mesenteric vein served as an acute exposure model of endotoxemia. In response to this challenge, a ninefold increase in hepatic ET-1 mRNA occurred within 3 h. The plasma level of immunoreactive ET-1 (irET-1) increased correspondingly by 8.5-fold within 6 h. ET-1 mRNA levels in liver endothelial cells (EC) isolated from livers of endotoxin-treated rats at various times after endotoxin challenge showed a more gradual increase. Northern blot analyses of the major liver cell types demonstrated that ET-1 mRNA was most abundant in the EC. The present results document a significant increase in the circulating level of irET-1 during episodes of endotoxemia. The increased hepatic ET-1 production in response to endotoxin infusion suggests that ET-1 produced in the liver could make a significant contribution to the plasma irET-1 and may be an important component in the hepatic responses to systemic trauma.

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