Abstract
Epidemiological studies have demonstrated that offspring born to mothers preeclampsia (PE) are at increased risk for developing cardiovascular diseases after birth, but the underlying mechanism is unknown. Angiotensin II receptor type 1 autoantibody (AT1-AA), an agonist acting via activation of the AT1 receptor, is believed to be involved in the pathogenesis of both PE and fetal growth restriction. The aim of the present study was to confirm the hypothesis that prenatal AT1-AA exposure increases the heart susceptibility to ischemia/reperfusion injury (IRI) in the offspring in an AT1-AA-induced animal model of PE, and determine whether or not the increase of maternal AT1-AA level is a factor contributing to sustained abnormalities of the heart structure during infancy. The hearts of 45-day-old offspring rats were studied using Langendorff preparation to determine the susceptibility of the heart to IRI. The results showed that the body weight of the maternal rats was not significantly different between the study and control groups, but the body weight of their offspring in AT1-AA group was decreased slightly at day 21 of gestational age, and at day 3 after birth. Although the heart weight index was not significantly affected at all ages examined, AT1-AA significantly increased the size of myocardial cells of the left ventricle (LV) at the age of 45 days. AT1-AA gained access to fetal circulation via the placenta and induced apoptosis of fetal myocardial cells. AT1-AA also significantly delayed recovery from IRI and affected the LV function of 45-day-old offspring. This was associated with a significant increase in IRI-induced LV myocardial infarct size. These results suggest that AT1-AA induced abnormal apoptosis of fetal myocardial cells during the fetal period and increased the cardiac susceptibility to IRI in adult offspring.
Highlights
Hypertension is a degenerative disease associated with aging, genetic, environmental and behavioral factors, but the etiological mechanism of hypertension has not been fully explained
Maternal and fetal general characteristics Maternal and fetal characteristics are described in Table 1, showing that there was no significant difference in initial Systolic blood pressure (SBP) and body weight of the pregnant rats
Body weight, heart weight, body length and placental weight were significantly smaller in fetal rats delivered by cesarean section that received a prenatal exposure to Angiotensin II receptor type 1 autoantibody (AT1-AA)
Summary
Hypertension is a degenerative disease associated with aging, genetic, environmental and behavioral factors, but the etiological mechanism of hypertension has not been fully explained. Evidence from both human and animal studies suggests that the hypertensive manifestations in adulthood are associated with environmental factors during fetal life. Evidence from both human and animal studies suggests that the hypertensive manifestations in adulthood are associated with environmental factors during fetal life1-3 This phenomenon is known as fetal origins of adult disease. Children born to mothers who smoke during pregnancy are at an increased risk of cardiovascular disease (CVD) [1]. A number of studies suggest an association between the risk of CVD and abnormal intrauterine growth, despite normal birth weight [5,6]
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