© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Growth hormone preserves cardiac sarcoplasmic reticulum Ca2+ release channels (ryanodine receptors) and enhances cardiac function in cardiomyopathic hamsters
Second Department of Internal Medicine, Yamaguchi University School of Medicine, Ube, Yamaguchi 755, Japan
* Corresponding author: Tel. 81-836-22-2248; Fax. 81-836-22-2246; e-mail: ohkusa@po.cc.yamaguchi-u.ac.jp
Objective: Growth hormone (GH) improves cardiac function in experimental models of heart failure and human dilated cardiomyopathy. However, the mechanism by which GH increases myocardial contractility is not entirely clear. Our aim was to examine the effects of GH on cardiac function and cardiac sarcoplasmic reticulum Ca2+ release channels (ryanodine receptors, RyR) in the hearts of UM-X7.1 cardiomyopathic hamsters during the development of heart failure. Methods: Experimental and healthy control hamsters were examined at the age of 20 weeks. Recombinant human GH (2 mg/kg/day, sc) or vehicle was then administered for 3 weeks. We examined (i) the in vivo left ventricular (LV) size and LV systolic function using transthoracic echocardiography, (ii) the density (Bmax) and affinity (Kd) of high-affinity [3H] ryanodine binding sites in crude homogenates from normal and cardiomyopathic hamster hearts. Results: Vehicle-treated UM-X7.1 hamsters exhibited significant increases in left ventricular end-diastolic diameter and end-systolic diameter (LVESd), and a significant decrease in LV fractional shortening (FS). GH-treatment attenuated the increase in LVESd and reduced the LV chamber size, and also significantly increased LVFS. Vehicle-treated UM-X7.1 hamsters exhibited a significantly lower Bmax than control hamsters (0.34±0.04 vs 0.44±0.06 pmol/mg, p<0.05), and the treatment with GH in UM-X7.1 hamsters significantly attenuated the reduction of Bmax {0.42±0.03 pmol/mg vs vehicle-treated group (0.34±0.04 pmol/mg), p<0.05}. Kd did not differ significantly between the experimental groups. In normal control hamsters, GH treatment with this dose did not significantly enhance LV systolic function or the density of RyRs. There was no significant difference in terms of the connective-tissue volume- fraction, myocyte size and capillary density between the GH- and vehicle-treated groups of UM-X7.1 hamsters. Conclusions: GH treatment may improve cardiac function by preserving the density of RyRs and enhancing cellular function in cardiomyopathic hamster hearts.
KEYWORDS Cardiomyopathic hamster; Growth hormone; Heart failure; Ryanodine receptor; Sarcoplasmic reticulum
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