Key result
Yttrium acetate slows heart contraction rate while altering mitochondrial calcium and potassium transport.
Why the study?
The effects of yttrium acetate on myocardium contraction and ion transport across the inner mitochondrial membrane in vertebrate heart tissue were not fully understood.
No immediate clinical implications; leaves open yttrium's effects on cardiac mitochondrial ion transport in vivo.
Inoptopic effect of yttrium acetate (Y 3+ ) on myocardium of the marsh frog Rana ridibunda and its effect on ion transport across the inner mitochondrial membrane (IMM) of rat heart was studied. Y 3+ was found to decrease the rate of heart contractions and to stimulate ion transport in the rat heart mitochondria in media with 10 mM glutamate and 2 mM malate. Presence of Y 3+ induced inhibition of energy-dependent Ca 2+ transport into mitochondria, which was expressed as a marked decrease of their swelling in the media containing 125 mM NH 4 NO 3 and Ca 2+ or 25 mM potassium acetate, 100 mM sucrose and Ca 2+ . It is suggested that the Y 3+ -induced decrease in rat muscle contractions is determined not only by direct suppressing effect of Y 3+ on potential-modulated Ca 2+ -channels of pacemaker and contractile cardiomyocytes (CM), but also by its indirect effect on Ca 2+ -carrier in IMM. The data confirming that Y 3+ activates energy-dependent K + transport catalyzed by mitochondrial uniporter and blocks Ca 2+ -channels in the mitochondrial membrane are important for more complete understanding of mechanisms of the Y 3+ action on vertebrates and human CM.
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Шемарова et al. (2014) studied this question. Yttrium acetate (Y3+) was evaluated on Rate of heart contractions and ion transport in mitochondria. Yttrium acetate decreased the rate of heart contractions and inhibited energy-dependent Ca2+ transport into mitochondria while activating energy-dependent K+ transport.
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