Noradrenergic subsensitivity of rat liver homogenates during chronic ethanol ingestion.
Prior studies indicated that chronic ethanol feeding induced noradrenergic subsensitivity of the cerebral cortex. Sensitivity was measured using the cAMP response of brain slices to norepinephrine (NE). In the present report we investigated the possibility that noradrenergic receptors in a visceral organ might be similarly affected by ethanol feeding. The cAMP response of liver homogenates to NE was measured. Chronic ethanol ingestion induced subsensitivity of the liver to NE similar to that observed in the brain. The ED50 was shifted to the right from 2.1 X 10(-5) M to 1.3 X 10(-4) M NE. By 3 days of ethanol withdrawal the cAMP response returned to control levels.
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000242:Cyclic AMP / Q000494:pharmacology; D004032:Diet; D000431:Ethanol / Q000494:pharmacology*; D006801:Humans; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects*; D008297:Male; D008930:Mitochondria, Liver / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D013375:Substance Withdrawal Syndrome / Q000378:metabolism; D013997:Time Factors
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D000431:Ethanol; D000242:Cyclic AMP; D009638:Norepinephrine