ABSTRACT
Recently, the thyroid hormone has been shown to cause increase in calcium ion (Ca(2+)) concentration by mobilizing intracellular calcium((2+)). The mobilization of intracellular calcium((2+)) in the absence of transmembrane calcium((2+)) influx has been accepted as evidence for a cell-surface Ca((2+))-receptor. The possible role of thyroid hormone in the regulation of cellular functions by ca((2+)-channel was investigated using parameters proven to indispensably involve Ca(2+). Bleeding and clotting times and rat uterine muscle activity in Ca(2+)-free Tyrode's solution. Adult female Wistar rats divided into four groups, namely; (i) Control, (ii) Thyroidectomized, (iii) Throidectomized-treated with thyroxine and (iv) Thyroxine-treated; were fed on rat chow. While groups i and ii were allowed access to tap water ad libitum for 60 days, groups iii and iv received tyroxine (10 mg/kg body weight) every alternate day and tap water ad libitum for 60 days. All groups were kept in an air-conditioned room till they were euthanized. The results showed that thyroxine elicited biphasic contraction in Ca (2+)-depletion and potentiated uterine contraction during Ca(2+)-loading (P < 0.001). Inhibition of contractions in thyroidectomy, showed dependency of Ca (2+) on thyroid hormones for the regulation of cellular functions.
