Longitudinal study of the renin-angiotensin-aldosterone system in hypertensive pregnant women: Deviations related to the development of superimposed preeclampsia

August, Phyllis; Lenz, Tomas; Aleš, Kathy L.; Druzin, Maurice L.; Edersheim, Terri G.; Hutson, J. M.; Miiller, Franco B; Laragh, John H.; Sealey, Jean E.

doi:10.1016/0002-9378(90)90639-o

Cited by 149 publications

(96 citation statements)

References 17 publications

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“…The absence of stimulation of the RAS in women developing hypertension during pregnancy or in women with preeclampsia has been confirmed by many studies [12]. The entire renin-angiotensin axis is affected in established preeclampsia, in particular, plasma renin concentrations are markedly decreased and there has been considerable recent interest in the possible role of alteration in the RAS in the pathophysiology of preeclampsia.…”

Section: Discussionmentioning

confidence: 88%

“…The entire renin-angiotensin axis is affected in established preeclampsia, in particular, plasma renin concentrations are markedly decreased and there has been considerable recent interest in the possible role of alteration in the RAS in the pathophysiology of preeclampsia. There is extensive evidence that plasma renin activity, plasma renin concentration, angiotensin II, angiotensinogen and plasma urinary aldosterone levels are all lower in preeclampsia compared with normotensive pregnant women [12]. Several laboratories have reported increased density of platelet AngII receptors and increased AngII binding in preeclamptic women compared to normal pregnant women [22].…”

Section: Discussionmentioning

confidence: 99%

“…During normal pregnancy the RAS is stimulated and plasma renin activity (PRA), angiotensinogen (AGT), angiotensin II (AngII) and aldosterone levels are increased [11]. However, in women who develop preeclampsia suppression of the RAS system has been observed [12]. Human linkage and association genetic studies have revealed the presence of polymorphisms in genes encoding key components of the RAS that account for the proportion of the variance in activity of this system [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Interaction between the polymorphisms of the renin–angiotensin system in preeclampsia

Bouba

Makrydimas

Kalaitzidis

et al. 2003

European Journal of Obstetrics & Gynecology and Reproductiv

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Preeclampsia is considered to be a multifactorial and multisystemic disorder with a genetic predisposition. Alterations in the reninangiotensin system are considered to play a significant role in the pathogenesis of the disease. In order to investigate the possible association of the three most common polymorphisms of the renin-angiotensin system genes with preeclampsia we have examined 41 women with preeclampsia and 102 normotensive pregnant women. DNA samples were genotyped for the M235T polymorphism of the angiotensinogen gene (AGT), the insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme gene (ACE) and the A1166C polymorphism of the angiotensin II type 1 receptor gene (AT1R) by PCR. Allele and genotype frequencies of the AGT gene polymorphism differed between the two study groups. The TT genotype of the M235T polymorphism was significantly increased in women who developed preeclampsia (P < 0:02). In addition, women with preeclampsia and TT genotype had more frequently the DD genotype or the 1166C allele than the control group showing a significant interaction between the genes. In conclusion, we found an association between the angiotensinogen variant 235T and preeclampsia as well as an interaction between the variant 235T and the two other genes studied. #

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Interaction between the polymorphisms of the renin–angiotensin system in preeclampsia

Bouba

Makrydimas

Kalaitzidis

et al. 2003

European Journal of Obstetrics & Gynecology and Reproductiv

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“…27 We intended to counteract this possible confounding variable by obtaining samples in the morning, at a time of the day when progesterone values are not increased. Other investigators have observed that circulating progesterone concentrations are increased in hypertensive women who subsequently develop PE 28 and in normotensive women around week 27, before the development of PE. 29 Several lines of evidence suggest that these changes might have a role in the development of PE.…”

Section: Hypertension February 2006mentioning

confidence: 90%

Time Course of Maternal Plasma Volume and Hormonal Changes in Women With Preeclampsia or Fetal Growth Restriction

et al. 2006

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Abstract-We tested the hypothesis that women with idiopathic fetal growth restriction (FGR) or preeclampsia (PE) have lower concentrations of some water-retaining hormones, such as aldosterone and estradiol, either preceding or concomitant with the onset of the reduced plasma volume described in these women. Plasma volume and serum concentrations of estradiol, progesterone, and aldosterone were measured serially at monthly intervals in 135 pregnant women from week 10 until term. Twenty-three developed idiopathic FGR, 17 had PE, and 95 remained normotensive and delivered normal-size infants (controls). Changes over time for each variable were studied using mixed models.Maternal age, parity, and weight/height at term were similar in all of the groups. Birth weight, body length, and ponderal index were lower in FGR and PE than in controls. Plasma volume increased throughout pregnancy in controls but was lower in FGR and PE from week 14 to 17 until term. Aldosterone values were lower in PE from week 26 to 29 onwards and in FGR after week 34. Progesterone concentrations were higher in PE than either control or FGR from week 18 to 21 until term. In contrast, FGR pregnancies had reduced progesterone and estradiol concentrations after week 34. Progesterone:estradiol ratio was significantly higher only in the PE group. In mothers with idiopathic FGR or PE, less expansion in plasma volume occurred before alterations in hormonal concentrations. We speculate that the early rise in progesterone may have a pathogenic role in the development of preeclampsia. Key Words: blood Ⅲ aldosterone Ⅲ preeclampsia Ⅲ estrogen P reeclampsia (PE) and fetal growth restriction (FGR) are frequent disorders of pregnancy and a leading cause of prenatal morbidity and mortality. In near-term pregnant women with either PE or FGR, we demonstrated lower plasma volume expansion, reduced cardiac output, and an increased total peripheral vascular resistance when compared with normotensive women who gave birth to normal-size infants. 1-3 Volume expansion during normal pregnancy seems to be secondary to renal and systemic vasodilatation that would activate the renin-angiotensin-aldosterone system that, in turn, would cause renal sodium and water retention. 4 -6 Estrogen production may also have a role in plasma volume expansion by stimulating hepatic angiotensinogen synthesis. 5,7 According to this proposed pathway for volume expansion, in the present study we tested the hypothesis that women with PE or FGR would have lower serum aldosterone and estradiol concentrations either preceding or concomitant with the onset of the reduced plasma volume. We measured plasma volume and hormonal concentrations in initially healthy pregnant women from weeks 10 to 13 until near term. After delivery, we compared the time course of these changes in control, FGR, and PE women. MethodsParticipants were women attending 2 prenatal clinics of the Southeastern Health Service of Santiago, Chile (Alejandro del Río and La Granja). These women belonged to a low-income population ...

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“…A study has reported that the effect may elevate the onset of overt hypertension by weeks to months [48]. In PE total plasma volume gets low [49] and probably increases circulating volume as evidenced by suppressed rennin and aldosterone [50, 51] and elevated natriuretic hormone compared to normal pregnancy [52]. The markers of endothelial activation and dysfunction like endothelin, cellular fibronectin, plasminogen activator inhibitor-1 (PAI-1) and von Willebrands factor are altered in PE.…”

Section: Pathophysiology Of Various Clinical Instancesmentioning

confidence: 99%

A Brief Overview of Preeclampsia

et al. 2013

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Preeclampsia (PE) is a leading cause of maternal mortality and morbidity worldwide. It occurs in women with first or multiple pregnancies and is characterized by new onset hypertension and proteinuria. Improper placentation is mainly responsible for the disease. If PE remains untreated, it moves towards more serious condition known as eclampsia. Hypertension, diabetes mellitus, proteinuria, obesity, family history, nulliparity, multiple pregnancies and thrombotic vascular disease contribute as the risk factors for PE. PE triggered metabolic stress causes vascular injury, thus contributing to the development of cardiovascular disease (CVD) and/or chronic kidney disease (CKD) in future. This risk appears to be increased especially in women with a history of recurrent PE and eclampsia. Clinically increased serum levels of sFlt-1 and decreased placental growth factor (PIGF) and vascular endothelial growth factor (VEGF) represent the severe condition of PE. The clinical findings of sever PE are assorted by the presence of systemic endothelial dysfunction, microangiopathy, the liver (hemolysis, elevated liver function tests and low platelet count, namely HELLP syndrome) and the kidney (proteinuria). The early detection of PE is one of the most important goals in obstetrics.

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Longitudinal study of the renin-angiotensin-aldosterone system in hypertensive pregnant women: Deviations related to the development of superimposed preeclampsia

Cited by 149 publications

References 17 publications

Interaction between the polymorphisms of the renin–angiotensin system in preeclampsia

Interaction between the polymorphisms of the renin–angiotensin system in preeclampsia

Time Course of Maternal Plasma Volume and Hormonal Changes in Women With Preeclampsia or Fetal Growth Restriction

A Brief Overview of Preeclampsia

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