Why the study?
Does altered thyroid status affect the size and rate dependence of outward potassium currents in rat ventricular myocytes?
Does altered thyroid status affect the size and rate dependence of outward potassium currents in rat ventricular myocytes?
Hypothyroidism attenuates transient outward potassium currents and alters their rate dependence in rat ventricular myocytes, effects that are reversible with T3 replacement.
Thyroid effects on rat myocyte K+ currents are hypothesis-generating; human studies needed before any clinical consideration.
The size and rate dependence of the transient (Ito) and steady-state (Iss) outward potassium currents were investigated in isolated rat ventricular myocytes obtained from euthyroid, hyperthyroid, and hypothyroid rats, using the whole cell, suction electrode voltage-clamp method. Under hypothyroid conditions Ito was reduced in size, with no significant change in Iss. In hypothyroid cells, the rate dependence of both currents was greatly enhanced, resulting in a much larger attenuation with increasing stimulation rates. A significant slowing of the recovery kinetics of Ito was observed. These effects of hypothyroidism were reversed by physiological triiodothyronine (T3) replacement. These current changes were reflected in an altered rate dependence of the action potential configuration in hypothyroid myocytes. Under hyperthyroid conditions no significant changes were observed in the amplitude or time course of recovery of Ito. Iss amplitude was increased, but no changes were found in its rate dependence. These results are discussed in terms of hormonal, long-term modulation of potassium currents, and in terms of cardiac pathology under conditions of altered thyroid status.
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Shimoni et al. (1995) studied this question.
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