Chronic ethanol inhibits receptor-stimulated phosphoinositide hydrolysis in rat liver slices.
The effects of chronic ethanol feeding on norepinephrine (NE)- and arginine-vasopressin (AVP)-stimulated phosphoinositide (PI) hydrolysis in rat liver slices was determined. The maximum NE-stimulated PI response was significantly reduced by 40% in liver slices from 8-month-old rats which had been treated for 5 months with a liquid diet containing ethanol compared to pair-fed controls. The maximum AVP-stimulated PI response was decreased by 39% in liver slices from the ethanol-fed rats compared to control. EC50 values for NE- and AVP-stimulated PI hydrolysis in liver slices were not affected by the chronic ethanol treatment. Similar reductions in the maximal NE- and AVP-stimulated PI hydrolysis (28% and 27%, respectively) were found in 22-month-old rats which had been maintained on an ethanol containing diet for 5 months compared to pair-fed controls. The binding of [3H]prazosin and [3H]AVP to liver plasma membranes from 8-month-old ethanol-fed rats was not significantly different from binding to liver membranes from sucrose-fed controls. Our data suggest that chronic ethanol ingestion may lead to a reduction in PI-linked signal transduction in liver.
Gonzales
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Department of Pharmacology, University of Texas, Austin 78712.
Crews
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D000375:Aging / Q000378:metabolism; D000437:Alcoholism / Q000378:metabolism*; D000818:Animals; D001127:Arginine Vasopressin; D006868:Hydrolysis / Q000187:drug effects; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism*; D008297:Male; D009638:Norepinephrine; D010716:Phosphatidylinositols / Q000378:metabolism*; D011224:Prazosin; D011869:Radioligand Assay; D051381:Rats; D011916:Rats, Inbred F344; D011956:Receptors, Cell Surface / Q000187:drug effects; D014316:Tritium
D010716:Phosphatidylinositols; D011956:Receptors, Cell Surface; D014316:Tritium; D001127:Arginine Vasopressin; D009638:Norepinephrine; D011224:Prazosin