The effects of the Ca2+ channel blockers verapamil, nifedipine, and diltiazem on 
triiodothyronine (T3) and thyroxine (T4) uptake were tested in cultured 
cardiomyocytes from 2-day-old rats. Experiments were performed at 37 degrees C 
in medium with 0.5% BSA for [125I]T3 (100 pM) or 0.1% BSA for [125I]T4 (350 pM). 
The 15-min uptake of [125I]T3 was 0.124 +/- 0.013 fmol/pM free T3 (n = 6); 
[125I]T4 uptake was 0.032 +/- 0.003 fmol/pM free T4 (n = 12). Neither T3 nor T4 
uptake was affected by 1% DMSO (diluent for nifedipine and verapamil). Uptake of 
[125I]T3 but not of [125I]T4 was dose dependently reduced by incubation with 
1-100 microM verapamil (49-87%, P < 0.05) or nifedipine (53-81%, P < 0.05). The 
relative decline in [125I]T3 uptake after 4 h of incubation with 10 microM 
verapamil or nifedipine was less than after 15 min or 1 h, indicating that the 
major inhibitory effect of the Ca2+ channel blockers occurred at the level of 
the plasma membrane. The reduction of nuclear [125I]T3 binding by 10 microM 
verapamil or nifedipine was proportional to the reduction of cellular [125I]T3 
uptake. Diltiazem (1-100 microM) had no dose-dependent effect on [125I]T3 uptake 
but reduced [125I]T4 uptake by 45% (P < 0.05) at each concentration tested. 
Neither the presence of 20 mM K+ nor the presence of low Ca2+ in the medium 
affected [125I]T3 uptake. In conclusion, the inhibitory effects of Ca2+ channel 
blockers on T3 uptake in cardiomyocytes are not secondary to their effects on 
Ca2+ influx but, rather, reflect interference with the putative T3 carrier in 
the plasma membrane.