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Effects of Chronic Ethanol Exposure on Cardiac Receptor‐Adenylyl Cyclase Coupling: Studies in Cultured Embryonic Chick Myocytes and Ethanol Fed Rats
Author(s) -
Blumenthal Roger S.,
Flinn Ian W.,
Proske Orm,
Jackson Donald G.,
Tena Rowena G.,
Mitchell Mack C.,
Feldman Arthur M.
Publication year - 1991
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1991.tb05215.x
Subject(s) - adenylyl cyclase , myocyte , ethanol , embryonic stem cell , medicine , endocrinology , microbiology and biotechnology , chemistry , embryo , coupling (piping) , embryogenesis , receptor , biology , biochemistry , materials science , gene , metallurgy
Ethanol effects in the brain appear to be mediated at least in part by an alteration In receptor‐effector coupling via guanine nucleotide‐binding regulatory proteins (G proteins). To test the hypothesis that a similar pathway participates in the cardlotoxic effects of ethanol, we assessed the effects of chronic ethanol on two commonly used experimental models: embryonic chick myocytes in culture and ven tricular myocardium from chronically fed rats. Ethanol had no effect on either the function or quantity of G proteins as assessed by effector‐stimulated adenylyl cyclase activity and the levels of ADP‐ribosylation substrates. In contrast, effector‐stimulated adenylyl cy clase activity was significantly altered in the liver of ethanol‐fed rats. These results suggest that receptor‐effector coupling via G proteins in our two cardiac models is insensitive to ethanol and that ethanol effects may be species or organ specific.