DEPENDENCE OF CALCIUM ON THYROID HORMONE FOR THE REGULATION OF CELLULAR FUNCTIONS

Recently, the thyroid hormone has been shown to cause increase in Ca²⁺ concentration by mobilizing intracellular Ca²⁺. The mobilization of intracellular Ca²⁺ in the absence of transmembrane Ca²⁺ influx has been accepted as evidence for a cell-surface Ca²⁺- receptor. The possible role of thyroid hormone in the regulation of cellular functions by Ca²⁺-channel was investigated using parameters proven to indispensably involve Ca²⁺: Bleeding and clotting times and rat uterine muscle activity in Ca²⁺-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 waterad libitum for 60 days, groups iii and iv received tyroxine (10mg/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 Ca²⁺- depletion and potentiated uterine contraction during Ca²⁺- loading (P<0.001). Inhibition of contractions in thyroidectomy, showed dependency of Ca²⁺ on thyroid hormones for the regulation of cellular functions.