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Objective(s): Thyroid hormones play an essential role in fetal growth and maternal hypo-thyroidism which leads to cardiovascular deficiency in their offspring. Considering this, we intended to investigate the impact of gestational hypothyroidism on offspring vascular contractibility and possible underlying mechanisms. Materials and Methods: Hypothyroidism was induced in female rats by administration of 6-n-propyl-2-thiouracil in drinking water (0.02%) till delivery. The offspring aorta smooth muscle (without endothelium) contractile response to KCl (10-100 mM), KCl in the presence of nifedipine (10-4-10-1 µM), phenylephrine (10-9-10-6 M) and finally, phenylephrine and caffeine 100 mM in Ca2+-free Krebs were measured. Results: KCl and phenylephrine-induced contractions were considerably lower in gestational hypothyroid (GH) than euthyroid offspring. GH responded to nifedipine with less sensitivity than control. The GH and control groups produced almost equal contraction in respond to phenylephrine and caffeine in Ca2+-free Krebs. Conclusion: This study suggests that in hypothyroid offspring L-type Ca2+ channels are less functional, while intracellular Ca2+ handling systems are less modified by low levels of maternal thyroid hormones.

Gestational hypothyroidism-induced changes in L-type calcium channels of rat aorta smooth muscle and their impact on the responses to vasoconstrictors