Hipotireoidismo materno e suas repercussões no controle autonômico da função cardiovascular e sensibilidade ao sódio em ratos adultos

Abstract

Introduction: Currently, it is known that internal and external stimuli to the intrauterine environment during fetal development can have important physiological consequences in the individual's adult life. Several studies have shown that different diseases in adulthood may have their origin in the early stages of life. A decrease in maternal thyroid hormone levels, as in gestational hypothyroidism (GHT) cases and during the lactation period, is related to problems in fetal heart development and long-term cardiovascular diseases. However, the mechanisms behind these effects are not yet fully understood. Objectives: Therefore, the aim of this work was to evaluate the cardiovascular consequences in adulthood caused by GHT during gestation and lactation periods and if these changes are related to the behavior of hydromineral intake. Material and methods: The study groups used were: Control, OMG (offspring treated with methimazole during the mother's gestation period), OML (offspring treated with methimazole during the mother's lactation period) and OMGL (offspring treated with methimazole during the mother's pregnancy and lactation period). We investigated this by measuring the arterial pressure, heart rate, baroreflex function and autonomic cardiovascular control of adult Wistar rats that underwent fetal and neonatal GHT. Results: As results, we found that the groups OMG and OMGL showed significantly less weight gain in the first 90 days after birth. These rats also presented an increase in both mean arterial pressure and systolic blood pressure, in addition to an increase of the sympathovagal index when compared to the control group. Regarding sodium sensitivity, our experiments showed that there was no difference and that the hemodynamic changes found are not due to the imbalance of sodium intake. Conclusion: In conclusion, our results showed that maternal thyroid hormone deficiency can chronically produce changes in cardiovascular function in the adult life of the offspring.