Chronic myocardial overload in rats causes a shift in creatine kinase isoenzymes towards fetal forms (MB and BB), suggesting an adaptive mechanism in hypertrophied myocytes.
Chronic overload due to an experimental abdominal aortic stenosis in rats causes hypertrophy of ventricles and a parallel increase of the MB and BB isoforms of creatine kinase (CK) in cardiac tissue. The CK isoenzyme profile was determined using a new two-step method combining anion exchange chromatography and electrophoresis. In overloaded ventricles a shift was observed from the MM isoform which decreased (from 407 +/- 10 mumol X min-1 X g-1 ww in sham-operated to 370 +/- 0.13, in the overloaded group, p less than 0.05) towards the MB and BB forms whose activity was enhanced (from 56 +/- 4 and 6.5 +/- 0.7 to 77 +/- 6 and 10.1 +/- 1.2, respectively, p less than 0.02). These modifications were more pronounced (318 +/- 15, 83 +/- 15 and 15.1 +/- 2.5, for the MM, MB and BB forms respectively, p less than 0.01) in rats having a very marked hypertrophy and whose ventricular/body weight ratio (expressed in mg of ventricles per g) was above 3. Moreover this ratio correlates both with the amount of the MB form (r = 0.32, p less than 0.05) and with the percentage of the B monomer (r = 0.51, p less than 0.01). This shift, like that previously described for lactate dehydrogenase and myosin, favoured the fetal form and this supports the hypothesis that overloaded myocytes improve their efficiency by expressing some of the isoforms normally present in the fetus.
Younes et al. (Tue,) studied this question.