Hypoxia-induced adaptational shift in MHC-beta isoform expression in rat ventricles

We investigated whether the shift of cardiac myosin heavy chain (MHC) isoform observed during exposure to hypoxia is secondary to hypertrophy, or whether it is directly related to the hypoxic stress. Twelve male Wistar-Kyoto rats, 14 weeks old, were randomly assigned to two groups: sea-level control group (CO) and hypoxia group (HX). The CO group was housed 4 weeks at 1,011 hPa, and the HX group was housed for 4 weeks at 701 hPa. The expression of MHC-beta was significantly increased (600%) in the HX group as compared to the CO group in the right ventricle (p < 0.01). An increased ventricular mass induced by hypoxic exposure was associated with an increased expression of MHC-beta in the right ventricle (p < 0.05). In the left ventricle, the MHC-b expression was significantly increased (295%) in the HX group as compared to the CO group without ventricular hypertrophy (p < 0.01). No differences were observed in the adenylyl cyclase activity or in the phosphodiesterase activities in both ventricles between the CO and HX groups (p > 0.05). Oxidative enzymatic activities (citrate synthase and three-hydroxyacyl-CoA dehydrogenase) were unchanged in both ventricles following 4 weeks of hypoxia (p > 0.05). These findings suggest that, besides cardiac hypertrophy, the hypoxia-induced adaptational change to the MHC-b isoform may be mediated through a specific mechanism related to the stress of hypoxia.