Differences in response of myosin isozyme transition of ordinary and specialized myocardium to overload.
To investigate the response of myosin isozyme transition in specialized myocardium to cardiac overload, we examined immunohistochemically the distribution of myosin isozymes in sinus node cells of overloaded canine atria, using the monoclonal antibodies CMA19 and HMC14, which are specific for atrial myosin heavy chain (alpha-HC) and ventricular myosin heavy chain (beta-HC), respectively. Overloading in canine right atria was induced by artificial tricuspid valve regurgitation and pulmonary stenosis. Right atrial mean pressure rose to 15-20 mm Hg (n = 4) 2 months after surgery. In the working myocardium, cardiac overload caused redistribution of myosin isozymes, alpha-HC to beta-HC. Compared with the normal right atria, fewer myocytes were labeled with CMA19, but more were labeled with HMC14. However, the reactivity of sinus node cells with CMA19 and HMC14 was not changed between normal and overloaded right atria, indicating no redistribution of myosin heavy chain isozymes, alpha-HC to beta-HC. These results suggest that isozymes in myosin heavy chains in the specialized myocardium are protected from overload effects by their firm cytoskeletal framework or other mechanisms.
Nomoto
K
K
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Komuro
I
I
Kuro-o
M
M
Tsuchimochi
H
H
Takaku
F
F
Machii
K
K
Yazaki
Y
Y
D000818:Animals; D006321:Heart / Q000503:physiopathology; D006325:Heart Atria; D006352:Heart Ventricles; D007150:Immunohistochemistry; D007527:Isoenzymes / Q000378:metabolism*; D009206:Myocardium / Q000166:cytology / Q000201:enzymology*; D009218:Myosins / Q000378:metabolism*; D011666:Pulmonary Valve Stenosis / Q000201:enzymology / Q000503:physiopathology; D012849:Sinoatrial Node / Q000166:cytology / Q000201:enzymology; D014262:Tricuspid Valve Insufficiency / Q000201:enzymology / Q000503:physiopathology
D007527:Isoenzymes; D009218:Myosins