Abstract：
OBJECTIVE: Maternal endothelial dysfunction in pregnancy hypertension is related to impairment of nitric oxide (NO) formation. However, NO levels and hemodynamic repercussions on the female offspring remain unclear. Therefore, this study hypothesized that maternal pregnancy hypertension reduces circulating NO metabolites and increases arterial blood pressure in first-generation offspring female rats.
METHODS: Descendant female rats were distributed in four groups as follows: virgin offspring of normotensive (VN) and hypertensive (VH) mothers and pregnant offspring of normotensive (PN) and hypertensive (PH) mothers. Hemodynamic and biochemical analyses were performed.
METHODS: The systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), and body weight were measured. NO metabolites in plasma, NO formation in human umbilical vein endothelial cells (HUVECs) incubated with plasma, and endothelial NO synthase (eNOS) expression in aortas were determined.
RESULTS: Increased SBP, DBP, and reduced HR were found on the 60 days of life in the VH group, whereas the PH group showed increased SBP and HR on pregnancy day 7. All groups showed no differences in body weight gain and eNOS expression. Plasma levels of NO metabolites were increased in the PN compared to the other groups. Increases in the NO formation were greater in HUVECs incubated with plasma from VN and PN groups compared to the VH and PH groups.
CONCLUSIONS: Female virgin and pregnant first-generation offspring rats from hypertensive pregnant mothers may have negative cardiovascular repercussions featured by increases in SBP, and possibly impaired NO formation is involved.
METHODS: Descendant female rats were distributed in four groups as follows: virgin offspring of normotensive (VN) and hypertensive (VH) mothers and pregnant offspring of normotensive (PN) and hypertensive (PH) mothers. Hemodynamic and biochemical analyses were performed.
METHODS: The systolic (SBP) and diastolic (DBP) blood pressure, heart rate (HR), and body weight were measured. NO metabolites in plasma, NO formation in human umbilical vein endothelial cells (HUVECs) incubated with plasma, and endothelial NO synthase (eNOS) expression in aortas were determined.
RESULTS: Increased SBP, DBP, and reduced HR were found on the 60 days of life in the VH group, whereas the PH group showed increased SBP and HR on pregnancy day 7. All groups showed no differences in body weight gain and eNOS expression. Plasma levels of NO metabolites were increased in the PN compared to the other groups. Increases in the NO formation were greater in HUVECs incubated with plasma from VN and PN groups compared to the VH and PH groups.
CONCLUSIONS: Female virgin and pregnant first-generation offspring rats from hypertensive pregnant mothers may have negative cardiovascular repercussions featured by increases in SBP, and possibly impaired NO formation is involved.
摘要：
目的：妊娠期高血压疾病的母体内皮功能异常与一氧化氮（NO）形成障碍有关。然而,对雌性后代的NO水平和血液动力学影响尚不清楚。因此,这项研究假设，在第一代后代雌性大鼠中，母体妊娠高血压会减少循环NO代谢产物并增加动脉血压。
方法：后代雌性大鼠分为以下四组：正常血压（VN）和高血压（VH）母亲的处女后代以及正常血压（PN）和高血压（PH）母亲的怀孕后代。进行血液动力学和生化分析。
方法：收缩压（SBP）和舒张压（DBP），心率(HR),并测量体重。血浆中的NO代谢物，与血浆一起孵育的人脐静脉内皮细胞（HUVECs）中的NO形成，并测定主动脉中内皮NO合成酶（eNOS）的表达。
结果：SBP增加，DBP,在VH组中，在60天的生命中发现HR降低，而PH组在妊娠第7天显示SBP和HR升高。所有组的体重增加和eNOS表达均无差异。与其他组相比，PN中NO代谢物的血浆水平升高。与VH和PH组相比,用来自VN和PN组的血浆孵育的HUVEC中NO形成的增加更大。
结论：来自高血压孕妇母亲的雌性处女和怀孕第一代后代大鼠可能具有以SBP升高为特征的负面心血管影响，并且可能涉及受损的NO形成。
方法：后代雌性大鼠分为以下四组：正常血压（VN）和高血压（VH）母亲的处女后代以及正常血压（PN）和高血压（PH）母亲的怀孕后代。进行血液动力学和生化分析。
方法：收缩压（SBP）和舒张压（DBP），心率(HR),并测量体重。血浆中的NO代谢物，与血浆一起孵育的人脐静脉内皮细胞（HUVECs）中的NO形成，并测定主动脉中内皮NO合成酶（eNOS）的表达。
结果：SBP增加，DBP,在VH组中，在60天的生命中发现HR降低，而PH组在妊娠第7天显示SBP和HR升高。所有组的体重增加和eNOS表达均无差异。与其他组相比，PN中NO代谢物的血浆水平升高。与VH和PH组相比,用来自VN和PN组的血浆孵育的HUVEC中NO形成的增加更大。
结论：来自高血压孕妇母亲的雌性处女和怀孕第一代后代大鼠可能具有以SBP升高为特征的负面心血管影响，并且可能涉及受损的NO形成。
