-transparent.png){kind=logo}
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.
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
June 1993,
Nihon rinsho. Japanese journal of clinical medicine,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
January 1987,
The American journal of cardiology,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
September 1994,
Circulation research,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
August 1993,
The American journal of physiology,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
March 1993,
Cardiovascular research,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
July 1982,
The Biochemical journal,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
April 1993,
Circulation research,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
January 1995,
Basic research in cardiology,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
February 2014,
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences,
J S Dool, and
A S Mak, and
P Friberg, and
H Wahlander, and
A Hawrylechko, and
M A Adams
January 2017,
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology,
