Although the overall shift towards the V3
myosin heavy chain (MHC) has been shown to be associated with
cardiac hypertrophy, quantitative evidence describing regional expression is sparse. The aim of this study was to compare and contrast the regional
ventricular myosin isoform expression in two distinct haemodynamic states: pressure and volume overload. Volume overload was achieved using an aortocaval
fistula (ACF) model and pressure overload by two-kidney-one-
clip (2K1C)
hypertension. A separate group (UC-2K1C) had the
clip removed 1 week prior to investigation.
Sham operated rats (
SHAM) served as controls. All groups were studied 4 weeks after surgery. Ventricular tissue samples (approximately 50 mg) were taken from the walls of the right ventricle (RV), septum and left ventricular (LV) free wall. Tissue samples (excluding RV) were divided into endocardium and epicardium, and
myosin expression was determined using
polyacrylamide gel electrophoresis.
Cardiac hypertrophy was substantial in both LV (1.7-fold) and RV (1.9-fold) in ACF rats. The 2K1C rats had similar LV enlargement (1.6-fold) whereas RV
hypertrophy was not as great (1.2-fold). Blood pressure (BP) was increased 65% in 2K1C rats, whereas there was no change in ACF rats with respect to
SHAM animals. After unclipping (UC-2K1C), LV
hypertrophy and BP had returned towards control levels. In general, V3 MHC expression was associated with increasing LV
hypertrophy in both 2K1C and ACF models. However, there was a marked endo-epi differential (1.5:1) in the LV free wall and septum of 2K1C rats. In contrast, in ACF rats there was no differential V3 MHC expression in the LV or septal tissue, i.e. expression was similar in both endo- and epi-samples. Elevated expression of V3 MHC persisted despite normotension and regression of
cardiac hypertrophy in UC-2K1C rats. Taken together with published results demonstrating that relative transmural myocyte
hypertrophy in ACF rats (endo > epi) is in contrast to that seen in 2K1C rats (epi > endo), the present findings reveal that regional V3
myosin expression represents a distinct adaptational component of the overall cardiac hypertrophic response in both volume and pressure overload.