The hyperthyroid state is associated with increased myocardial contractility. To clarify responsible mechanisms, we examined the effects of thyroid hormone on slow Ca channels, beta-adrenergic receptors, transsarcolemmal 45Ca flux and cytosolic free calcium in cultured chick ventricular cells. Compared with cells grown without triiodothyronine (T3), cells grown in 10 nM T3 possessed (a) 67% (P < 0.05) more dihydropyridine 3H-PN200-110 binding sites, (b) 24% (P < 0.05) more beta-adrenergic antagonist 3H-CGP12177 binding sites, (c) a 57% (P < 0.05) greater nifedipine-sensitive initial 45Ca uptake rate, and (d) a 31% (P < 0.05) greater nifedipine-sensitive 45Ca uptake rate in response to BAY k 8644. Time-averaged mean intracellular free Ca concentration ([Cali) measured with fura-2, total protein content,

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