Chronic alcohol-induced changes in cardiac contractility are not due to changes in the cytosolic Ca 2+ transient

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 275; no. 1; pp. H122 - H130
• Main Authors: Figueredo, Vincent M, Chang, Kevin C, Baker, Anthony J, Camacho, S Albert
• Format: Journal Article
• Language: English
• Published: United States 01.07.1998
• Subjects: adenosinetriphosphatase; myosin heavy chain; phospholamban; ethanol; myocyte; sarcoplasmic reticulum
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.1998.275.1.H122

Long-standing heavy alcohol consumption acts as a chronic stress on the heart. It is thought that alcohol-induced changes of contractility are due to altered Ca handling, but no measurements of cytosolic Ca ([Ca ] ) after chronic alcohol exposure have been made. Therefore experiments were performed to determine whether alcohol-induced changes in contractility are due to altered Ca handling by measuring [Ca ] (indo 1) in hearts from rats drinking 36% ethanol for 7 mo and age-matched controls. Peak left ventricular pressure was depressed (-16%), whereas rates of contraction (12%) and relaxation (14-20%) were faster in alcohol-exposed hearts. Systolic [Ca ] (808 ± 45 vs. 813 ± 45 nM), diastolic [Ca ] (195 ± 11 vs. 193 ± 10 nM), and rates of [Ca ] rise and decline were the same in alcohol-exposed and control hearts. Protein levels of Ca -handling proteins, sarcoplasmic reticulum Ca -ATPase and phospholamban, were the same in myocytes isolated from alcohol-exposed and control hearts (SDS-polyacrylamide gel). These data suggest that chronic alcohol-induced contractile changes are not due to altered Ca handling but may be due to changes at the level of the myofilament. As a first step in elucidating the mechanism(s) of alcohol-induced changes at the myofilament, we assessed myosin heavy chain (MHC) isoform content (SDS-polyacrylamide gel). α-MHC was decreased relative to β-MHC ( a/ a+ b = 0.55 ± 0.03 vs. 0.66 ± 0.02; P < 0.02) in alcohol-exposed hearts, which cannot account for the observed alcohol-induced contractile changes. In conclusion, changes of myocardial contractility due to chronic alcohol exposure do not result from altered Ca handling but from changes at the level of the myofilament that do not involve MHC isoform shifts.