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Cardiovascular Research 2006 69(1):140-151; doi:10.1016/j.cardiores.2005.07.010
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Copyright © 2005, European Society of Cardiology

Spontaneous diastolic contractions and phosphorylation of the cardiac ryanodine receptor at serine-2808 in congestive heart failure in rat

Masakazu Obayashia, Bailong Xiaob, Bruno D. Stuyversb, Allen W. Davidoffb, Jie Meib, S.R. Wayne Chenb and Henk E.D.J. ter Keursb,*

aDepartment of Medical Bio-regulation, Division of Cardiovascular Medicine, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan
bDepartments of Medicine, Physiology and Biophysics, Health Sciences Center, University of Calgary, Calgary, Alberta, Canada

* Corresponding author. Department of Physiology/Biophysics, University of Calgary, 3330 Hospital Drive, NW, Calgary, Alberta, Canada, T2N 4N1. Tel.: +1 403 289 7156; fax: +1 403 270 0313. Email address: terkeurs{at}ucalgary.ca

Objective: The role of phosphorylation of the ryanodine receptor at serine-2808 (RyRS2808) in congestive heart failure (CHF) is controversial, and effects of RyRS2808 phosphorylation on contraction are unclear. It has been reported that diastolic sarcomere length (SL) fluctuations accompany propagating contractile waves due to propagating SR Ca2+ release in trabeculae from rats with CHF. Here, we studied the influence of RyR destabilization by FK506 and isoproterenol on twitch force (Ftw) and SL fluctuations in right ventricular (RV) trabeculae. We measured phosphorylation of RyRS2808 in rats with myocardial infarction (MI) with or without β-blockade and in rats during isoproterenol stimulation in order to assess the role of RyRS2808 phosphorylation in SL fluctuations in failing hearts.

Methods: Five groups of male Lewis Brown–Norway rats were studied 3 months after MI: i) Sham; ii) MI with CHF (cMI); iii) MI without CHF; iv) metoprolol-treated MI, with and without CHF. The root mean square (RMSSL) of SL fluctuations in RV trabeculae was calculated.

Results: RMSSL increased strongly both following a short train of stimuli at 2.5 Hz and following catecholamine activation in trabeculae from MI with CHF, resulting in a decrease in Ftw in proportion to RMSSL. RyRS2808 phosphorylation was increased significantly in the left ventricle (LV; ~58%, P<0.05) but not in the RV (n.s.) in MI rats with CHF. FK506 tripled high frequency stimulation-induced RMSSL in nonfailing trabecula but did not further enhance RMSSL in failing trabecula. Isoproterenol increased RMSSL in nonfailing trabeculae only modestly despite a substantial increase in RyRS2808 phosphorylation in the RV (~60%, P<0.05). Isoproterenol induced SL fluctuation without an increase in RV-RyRS2808 phosphorylation in failing trabeculae. Chronic β-blockade decreased high frequency and catecholamine stimulation-induced RMSSL while RyRS2808 phosphorylation in the RV was indistinguishable from that in cMI.

Conclusions: Acute RyRS2808 phosphorylation by itself does not cause spontaneous contractile waves owing to RyR2 destabilization. Spontaneous contractile waves in CHF are not caused by RyRS2808 phosphorylation alone, suggesting that factors other than RyRS2808 phosphorylation affect RyR function.

KEYWORDS Ca2+; Contractile function; E–C coupling; Heart failure; Infarction

Time for primary review 29 days


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