Hemodynamic properties and arterial structure in male rat offspring with fetal hypothyroidism

Abstract

Abstract. Thyroid hormones (THs) play a crucial role in the development of different systems during fetal life; fetal hypothyroidism (FH) is associated with reduced cardiac function and dimensions in neonates. The aim of this study is to determine whether TH deficiency during fetal life is associated with arterial structural and hemodynamic changes during adulthood. Hypothyroidism was induced by adding 0.025% 6-propyl-2-thiouracil in drinking water throughout pregnancy, while controls consumed only tap water. Hemodynamic parameters, cross-sectional area, intima-media thickness (IMT), and density of nuclei of smooth muscle cells and endothelial cells (ECs) in the aorta and mesenteric arteries were measured. Compared to controls, in the FH group, baseline systolic blood pressure (105.7 ± 3.1 vs. 87.9 ± 3.3 mm Hg, p < 0.01), diastolic blood pressure (64.4 ± 1.7 vs. 53.2 ± 2.1 mm Hg, p < 0.05), and mean arterial pressure (80.9 ± 2.1 vs. 67.1 ± 2.1 mm Hg, p < 0.01) were significantly lower. In addition, in the FH group, intensity and latency of response to phenylephrine were significantly lower and longer, respectively, as were the IMT and density of ECs in the aorta and superior mesenteric arteries. In conclusion, this study showed that TH deficiency during fetal life can have long-lasting functional and histological effects, which can compromise cardiovascular function during adulthood.

Antenatal/early postnatal hypothyroidism increases the contribution of Rho-kinase to contractile responses of mesenteric and skeletal muscle arteries in adult rats

“…9,10 Of note, already at the age of 6 weeks, the progeny of PTU-treated dams demonstrated restored blood levels of thyroid hormones and TSH, 20 which is consistent with other studies, where the restoration of thyroid state was observed in 4 weeks after PTU withdrawal. 8 Based on the above, we can consider that the adult rats from PTU group had an euthyroid status for at least 4 weeks before their arteries were taken for in vitro studies.…”

“…7 On the other hand, high blood pressure does not always develop in adult progeny of hypothyroid rats. 8,9 The diversity of results suggests that there are adverse circulatory alterations only in certain organs, which might be more susceptible to the developmental thyroid deficiency than others. For example, antenatal/early postnatal hypothyroidism causes increased contractility of coronary vasculature in adult rats, despite the absence of evident alterations in their thyroid function and blood pressure level.…”

Transient Congenital Hypothyroidism Alters Gene Expression of Glucose Transporters and Impairs Glucose Sensing Apparatus in Young and Aged Offspring Rats

“…Ghanbari et al have shown that offspring rats with TCH had lower serum TT 4 and TT 3 until days 14 and 21 after birth, respectively, despite their thyroid hormone levels being comparable to normal rats 90 days after birth [59]. Mooradian et al have reported that thyroid hormones have different effects on GLUTs expression during development and in adulthood [32].…”

“…It has also been reported that adult hypothyroidism had no effect on GLUT2 and GcK expression in both islets and liver [70, 71]. In this study, we used a transient model of CH, where thyroid hormone levels were similar to normal rats, whereas adult hypothyroid rats usually have lower than normal levels of thyroid hormones [59]. …”

Changes in Endothelial Nitric Oxide Production in Systemic Vessels during Early Ontogenesis—A Key Mechanism for the Perinatal Adaptation of the Circulatory System

“…Importantly, in many mammalian species the blood concentration of thyroid hormones was shown to be higher during the early stages of development compared to adulthood. For example, a rise in blood triiodothyronine (T 3 ) concentration was shown between gestational week 30 and birth in humans and between birth and the 3rd postnatal week in rats [49,50]. Thyroid hormones can have rapid and long-term effects on eNOS expression and/or activity in endothelial cells (Figure 1).…”