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Am J Physiol Heart Circ Physiol 280: H2046-H2052, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 5, H2046-H2052, May 2001

Impaired sarcoplasmic reticulum function leads to contractile dysfunction and cardiac hypertrophy

Markus Meyer1, Susanne U. Trost1, Wolfgang F. Bluhm1, Harm J. Knot2, Eric Swanson1, and Wolfgang H. Dillmann1

1 Department of Medicine, University of California, San Diego, California 92093; and 2 Department of Medicine, University of Vermont, Burlington, Vermont 05405

Sarcoplasmic reticulum (SR)-mediated Ca2+ sequestration and release are important determinants of cardiac contractility. In end-stage heart failure SR dysfunction has been proposed to contribute to the impaired cardiac performance. In this study we tested the hypothesis that a targeted interference with SR function can be a primary cause of contractile impairment that in turn might alter cardiac gene expression and induce cardiac hypertrophy. To study this we developed a novel animal model in which ryanodine, a substance that alters SR Ca2+ release, was added to the drinking water of mice. After 1 wk of treatment, in vivo hemodynamic measurements showed a 28% reduction in the maximum speed of contraction (+dP/dtmax) and a 24% reduction in the maximum speed of relaxation (-dP/dtmax). The slowing of cardiac relaxation was confirmed in isolated papillary muscles. The late phase of relaxation expressed as the time from 50% to 90% relaxation was prolonged by 22%. After 4 wk of ryanodine administration the animals had developed a significant cardiac hypertrophy that was most prominent in both atria (right artrium +115%, left atrium +100%, right ventricle +23%, and left ventricle +13%). This was accompanied by molecular changes including a threefold increase in atrial natriuretic factor mRNA and a sixfold increase in beta -myosin heavy chain mRNA. Sarcoplasmic endoplasmic reticulum Ca2+ mRNA was reduced by 18%. These data suggest that selective impairment of SR function in vivo can induce changes in cardiac gene expression and promote cardiac growth.

growth; inotropic agents; myocardial contraction; Ca2+ handling; endothelial cell coupling


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