Key result
Cyclosporin A decreases maximal ryanodine binding and increases dissociation constant in rat cardiac sarcoplasmic reticulum.
Why the study?
Chronic cyclosporin A treatment was reported to induce reversible alterations of contractile properties in rat hearts, but the underlying molecular mechanisms remained to be defined.
Does cyclosporin A alter the characteristics of the Ca2+-release channel in cardiac sarcoplasmic reticulum in rats?
Population
Rats
Comparison
Cyclosporin A treatment vs control
Design
Preclinical animal study
Follow-up
3 wk
Authors
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Does not support clinical practice changes; leaves open calcineurin-mediated effects on human cardiac contractility.
Does cyclosporin A alter the characteristics of the Ca2+-release channel in cardiac sarcoplasmic reticulum in rats?
Cyclosporin A induces heart muscle-specific alterations of the Ca2+-release channel, likely via calcineurin upregulation, which may explain its effects on cardiac contractile properties.
Park et al. (1999) studied this question. Cyclosporin A vs. control was evaluated on ryanodine binding (Bmax) and dissociation constant (Kd). Cyclosporin A treatment (15 mg/kg/day for 3 weeks) in rats decreased maximal ryanodine binding and increased the dissociation constant of ryanodine in cardiac sarcoplasmic reticulum.
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