A comparative investigation into the effect of chronic alcohol feeding on the myocardium of normotensive and hypertensive rats: An electrophoretic and biochemical study
Vb. Patel et al., A comparative investigation into the effect of chronic alcohol feeding on the myocardium of normotensive and hypertensive rats: An electrophoretic and biochemical study, ELECTROPHOR, 21(12), 2000, pp. 2454-2462
We investigated whether the imposition of chronic alcohol in hypertension l
eads to greater biochemical and cellular abnormalities of the myocardium th
an those arising in normotension. Fifteen-week-old spontaneously hypertensi
ve rats (SHR) and Wistar Kyoto (WKY) rats were fed ethanol-containing diets
for six weeks. Particular attention was focused on the composition of cont
ractile proteins identified by sodium dodecyl sulfate-polyacrylamide gel el
ectrophoresis (SDS-PAGE), fractional rate of protein synthesis, and synthes
is rates relative to RNA (RNA activity) or DNA (cellular efficiency). In ad
dition, myocardial enzymes and adenine nucleotides were measured. In both S
HR and WKY rats chronic ethanol caused a general decrease in the contents o
f all nine contractile proteins with myosin heavy chain predominantly affec
ted. Fractional rates of mixed (i.e., total) and myofibrillary proteins rem
ained unaltered in both WKY rats and SHR, as were cellular efficiencies. Th
e RNA activity was significantly reduced in ethanol-treated SHR but not in
WKY rats. In ethanol-treated SHR, cardiac creatine kinase (CK) and malate d
ehydrogenase (MDH) activities were increased, AMP levels were elevated, whi
lst ATP levels and the energy charge were reduced. In WKY rats, the only si
gnificant change related to increased aspartate aminotransferase activities
in response to alcohol feeding. Although there were only subtle difference
s between the response of the normotensive and hypertensive rats due to eth
anol dosage, the reduced ATP levels and increased CK and MDH activities in
SHR may reflect a greater susceptibility to ischaemic damage. Reduced contr
actile protein content, particularly myosin heavy chain, may contribute to
contractile defects, a common feature of subclinical and clinical alcoholic
cardiomyopathy.