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J. Biol. Chem., Vol. 265, Issue 29, 17432-17435, 10, 1990
CR Gandhi, K Stephenson and MS Olson
Endothelin, a peptide mediator produced by vascular endothelial cells,
caused sustained vasoconstriction of the portal vasculature in the perfused
rat liver. The vasoactive effect of endothelin was accompanied by increased
glycogenolysis and alterations in hepatic oxygen consumption. The
endothelin-induced increase in the portal pressure was
concentration-dependent with an EC50 of 1 nM. Endothelin-induced hepatic
glycogenolysis was dose-dependent but exhibited a different EC50 than for
the vasoconstrictive effects of endothelin. Hepatic vasoconstriction and
glycogenolysis following endothelin infusion were inhibited when Ca2+ was
removed from the perfusion medium. The endothelin-induced responses in the
liver were not altered by prior infusion of phenylephrine (alpha-adrenergic
agonist), isoproterenol (beta-adrenergic agonist), angiotensin II,
glucagon, platelet- activating factor, or the platelet-activating factor
antagonist, BN52021. However, repeated infusion of endothelin resulted in
desensitization of the glycogenolytic response but was without a
significant effect on hepatic vasoconstriction. Endothelin also stimulated
metabolism of inositol phospholipids in isolated hepatocytes and Kupffer
cells in primary culture. The present experiments demonstrate, for the
first time, that endothelin is a very potent agonist in the liver eliciting
both a sustained vasoconstriction of the hepatic vasculature and a
significant increase in hepatic glucose output.
Endothelin, a potent peptide agonist in the liver
Department of Biochemistry, University of Texas Health Science Center, San Antonio 78284.
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