Key result
Hyperthyroidism reduces myocardial calcium channel density, whereas hypothyroidism shows no effect in preclinical models.
Why the study?
The regulation of calcium channel binding site density by thyroid hormone in myocardial and brain tissues and its relation to myocardial hypertrophy was unclear.
Answers are grounded in this paper and cite their sources.
May inform thyroid and adrenergic effects on rat myocardial calcium channels; leaves open human relevance or therapeutic implications.
The density of calcium channel binding sites as determined by [3H]-nitrendipine binding was found to be decreased in hearts of hyperthyroid rats but hardly altered by hypothyroidism. In contrast, dihydropyridine binding sites in the cerebral cortex were unaffected by dysthyroid states. Myocardial [3H]-nitrendipine binding sites were also decreased after treatment of the animals with isoprenaline but not in spontaneously hypertensive rats. These findings suggest that myocardial hypertrophy is not necessarily accompanied by a loss of calcium channels and that thyroid hormone regulates the density of [3H]-nitrendipine binding sites in a tissue-specific manner.
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Kosiński et al. (1990) studied Hypo- and hyperthyroidism (animal model). Hypothyroidism and hyperthyroidism vs. Normal thyroid state (implied) was evaluated on Density of calcium channel binding sites ([3H]-nitrendipine binding) in myocardial and brain membranes. Hyperthyroidism decreased the density of myocardial calcium channel binding sites in rats, whereas hypothyroidism had no effect, suggesting tissue-specific regulation by thyroid hormone.
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