Abstract
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 water ad 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.
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