One-sided ventricular overload in rats induced significant beta-MHC messenger RNA and protein expression only in the overloaded ventricle, not the unloaded ventricle, compared to sham-operated rats.
It is uncertain whether the shift of cardiac myosin heavy chain (MHC) during pressure overload can be induced by some intrinsic factors or by the stress imposed directly on the individual myocytes. To study whether the changes in cardiac MHC gene expression produced by one-sided overload are limited to the involved ventricle or extend to the other ventricle, we examined MHC gene expression and isozyme transition in the left and right ventricles in aortic coarctated and pulmonary artery-banded rats. It has been confirmed that the pressure overload is indeed limited to the loaded ventricle. The results showed that, compared with sham-operated rats, there was no significant induction of the beta-MHC messenger RNA and corresponding protein in the unloaded ventricle, whereas significant induction was observed in the overloaded ventricle. These results demonstrated that the changes in MHC gene expression and isozyme produced by one-sided ventricular overload are limited to the involved ventricle. We conclude that the MHC gene regulation during hemodynamic overload may not be induced by intrinsic factors, such as hormones, catecholamine, or atrial natriuretic peptide, but is induced by direct local response to increased load.
Imamura et al. (Sun,) conducted a other in Cardiac overload. One-sided ventricular overload (aortic coarctation or pulmonary artery banding) vs. Sham-operated rats was evaluated on MHC gene expression and isozyme transition (beta-MHC mRNA and protein). One-sided ventricular overload in rats induced significant beta-MHC messenger RNA and protein expression only in the overloaded ventricle, not the unloaded ventricle, compared to sham-operated rats.