Raised prorenin and renin concentrations in pre-eclamptic placentae when measured after acid activation

Singh, Harbindar Jeet Singh Gurcharan; Rahman, Abdul Malek Abdul; Larmie, E. T.; Nila, A.

doi:10.1016/j.placenta.2004.01.013

Cited by 21 publications

(9 citation statements)

References 48 publications

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“…Herse et al 22 also found a trend for elevated renin expression in preeclamptic placental tissue. Measurements of total renin concentration and active renin were significantly higher in preeclamptic placentas, 36 which corroborates our data showing a possible trend for increased renin mRNA in the preeclamptic chorionic villi.…”

Section: Discussionsupporting

confidence: 91%

Activation of Local Chorionic Villi Angiotensin II Levels But Not Angiotensin (1-7) in Preeclampsia

et al. 2008

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Abstract-The chorionic villi in the placenta are responsible for the regulation of fetal oxygen and nutrient transport.Although the peripheral renin-angiotensin system is activated during normal pregnancy, the regulation of the local chorionic villi renin-angiotensin system remains unknown. Therefore, placental chorionic villous tissue was collected from nulliparous third-trimester normotensive or preeclamptic subjects and was analyzed for angiotensin peptide content, angiotensinogen, renin, angiotensin-converting enzyme (ACE), ACE2, neprilysin, angiotensin II type 1 (AT 1 ), angiotensin II type 2, Mas receptor mRNAs, and angiotensin receptor density and subtype. Angiotensin II in chorionic villi was significantly higher in preeclamptic subjects, whereas angiotensin (1-7) was not different. Key Words: preeclampsia Ⅲ renin angiotensin system Ⅲ pregnancy Ⅲ placenta Ⅲ angiotensin receptors Ⅲ Mas receptor Ⅲ angiotensin (1-7) P reeclampsia, a hypertensive disorder of pregnancy, is clinically defined as maternal hypertension, proteinuria, and generalized edema occurring after the 20th week of gestation. Preeclampsia is the second leading cause of maternal mortality in the United States, affecting 7% to 10% of all pregnancies and contributing significantly to stillbirths and neonatal morbidity and mortality. 1 Thus, the prevention of preeclampsia would have a significant impact on maternal and neonatal outcome. Nevertheless, the pathophysiology of preeclampsia remains poorly understood. Although preeclampsia is often considered a multisystem disorder, one of the postulated pathological features of this disease is an impaired maternal uterine spiral artery remodeling. In preeclampsia, there is a decrease of embryonic trophoblast cell invasion of the uterine spiral arteries, which, in turn, prevents the diameter of these arteries from expanding and consequently leads to a reduction of blood flow into the placenta. 2,3 Without the remodeling of the uterine vasculature, the placenta becomes hypoxic as gestation advances, resulting in an oxygen deficiency within the tissue. The hypoxic placenta can then release factors into the maternal circulation that result in generalized endothelial dysfunction, vascular inflammation, and proteinuria. [3][4][5] Although several factors, including soluble fms-like tyrosine kinase 1 6 and soluble endoglin, 7 were discovered recently to play a role in the pathogenesis of preeclampsia, there are still many unanswered questions in the development of this disease.The renin-angiotensin system (RAS) is an important regulator of blood pressure, sodium, and fluid homeostasis and has been shown previously to play a role in preeclampsia. In normal pregnancy, estrogen causes an overexpression of the RAS by increasing both tissue and circulating levels of angiotensinogen 8,9 and renin. 10 -13 Consequently, plasma angiotensin (Ang) II is increased in association with the rise of angiotensinogen and plasma renin activity during gestation. 14,15 Normal pregnant women are resistant to the pressor effects...

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Section: Discussionsupporting

confidence: 91%

Activation of Local Chorionic Villi Angiotensin II Levels But Not Angiotensin (1-7) in Preeclampsia

et al. 2008

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“…Renin mRNA was found to be present in normal and gestational hypertension placenta, besides that, no significant difference of its mRNA and protein levels was found in normal versus gestational hypertension, which is consistent with some previous reports in normal versus preeclamptic [22]. On the contrary, in the study of Singh et al [26] total renin concentration and active renin were significantly higher in preeclamptic placentas. The different results may indicate a possible trend for increased renin mRNA in the development from gestational hypertension to preeclamptic.…”

Section: Discussionsupporting

confidence: 89%

Regulation of renin-angiotensin system in gestational hypertension

Jin¹,

Zhang²,

Zhu³

et al. 2017

Obstet Gynecol Rep

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Background: Hypertension is common disease amongst women with pregnancy. It is associated with significant maternal, fetal and infant morbidity. Current research on the mechanism of the hypertensive disorders is limited. The Renin-Angiotensin System (RAS) is a hormone signaling cascade that regulates blood pressure and systemic electrolyte and fluid balance. Our study was designed to focus on the mechanism of gestational hypertension before preeclampsia occurred, exploring the change in both circulating RAS and local RAS.

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“…Interestingly, high total renin levels have been found in several clinical settings characterized by endothelial dysfunction such as heart failure [34] , preeclampsia [35] , diabetic nephropathy [36][37][38][39] and retinopathy [40][41][42] . Therefore, it is likely that increased total renin levels may also contribute to endothelial dysfunction, a known abnormality in patients with PCOS [43][44][45] .…”

Section: Discussionmentioning

confidence: 99%

Hyperreninemia Characterizing Women with Polycystic Ovary Syndrome Improves after Metformin Therapy

Diamanti-Kandarakis

Economou²,

Livadas³

et al. 2009

Kidney Blood Press Res

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Background: Polycystic ovary syndrome (PCOS) is characterized by chronic anovulation, hyperandrogenemia and insulin resistance. Hyperreninemia is observed in insulin resistance and hyperandrogenemic states. Aims: To investigate the levels of total plasma renin and their possible relationship with insulin resistance and hyperandrogenemia and to explore the effect of metformin on these parameters in PCOS women. Methods: 48 PCOS women who were age- and body mass index (BMI)-matched with 21 healthy women were studied. Total renin, aldosterone levels, glucose and insulin levels were measured at basal state and during an oral glucose tolerance test in all subjects. A subgroup of women with PCOS was evaluated 6 months after metformin administration. Results: Total renin levels were significantly higher in PCOS women compared to controls. PCOS women compared to controls displayed higher areas under the curve for glucose, insulin and total renin (AUCREN). Mean AUCREN was correlated significantly with insulin resistance indices and positively with free testosterone levels. Total renin, aldosterone, androgen levels and insulin sensitivity indices were significantly improved after 6 months on metformin treatment. Conclusions: PCOS women demonstrated an insulin resistance and hyperandogenemia-related increase in serum total renin levels. Metformin treatment was shown to significantly reduce total renin levels.

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Raised prorenin and renin concentrations in pre-eclamptic placentae when measured after acid activation

Cited by 21 publications

References 48 publications

Activation of Local Chorionic Villi Angiotensin II Levels But Not Angiotensin (1-7) in Preeclampsia

Activation of Local Chorionic Villi Angiotensin II Levels But Not Angiotensin (1-7) in Preeclampsia

Regulation of renin-angiotensin system in gestational hypertension

Hyperreninemia Characterizing Women with Polycystic Ovary Syndrome Improves after Metformin Therapy

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