Distribution of Angiotensin-(1-7) and ACE2 in Human Placentas of Normal and Pathological Pregnancies

Valdés, Gloría; Neves, Liomar A. A.; Anton, Lauren; Corthorn, Jenny; Chacón, Cecília; Germaín, A; Merrill, David; Ferrario, Carlos M.; Sarao, Renu; Penninger, Josef; Brosnihan, K. Bridget

doi:10.1016/j.placenta.2005.02.015

Cited by 243 publications

(272 citation statements)

References 37 publications

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“…22,23 Although speculative, we postulate that an adequate maternal endothelial function represents a prerequisite for the reception of the invasive trophoblasts by the spiral arteries, which modify their morphology and replace their endothelium. A spiral artery healthy endothelium supposedly constitutes the target of the vasodilator factors synthesized by approaching trophoblasts (NO, bradykinin, and angiotensin-(1-7) among others 41,42 ).…”

Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction

et al. 2007

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Abstract-We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, L-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (nϭ22), patients with severe preeclampsia (nϭ25), or patients with recurrent pregnancy loss (nϭ29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endotheliumindependent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, L-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated. Key Words: endothelial dysfunction Ⅲ endothelium-mediated vasodilatation Ⅲ pregnancy Ⅲ preeclampsia Ⅲ recurrent abortion Ⅲ cardiovascular risk P reeclampsia not only elevates obstetric morbidity and mortality, but also places the mother at increased risk for developing cardiovascular disease (CVD) later in life. Indeed, subjects with preeclampsia are susceptible to hypertension, obesity/metabolic syndrome, and to CVD particularly if the preeclampsia is complicated by preterm birth. [1][2][3][4] Interestingly, subjects with recurrent spontaneous abortions have also been reported to be at increased risk for the development of cerebrovascular disease later in life. 5 This suggests that there may be underlying risk factors of CVD that predispose to both preeclampsia and/or spontaneous abortions, 2 conditions that represent different degrees of placentation defects.One potential unifying mechanism could involve the presence of endothelial dysfunction before the obstetric complication. Maternal endothelial dysfunction could impair the invasion of extravillous trophoblasts into the spiral arter...

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Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction

et al. 2007

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“…In human placenta, we showed pronounced immunocytochemical expression of ACE2 and Ang-(1-7) and specific staining in cytotrophoblast, syncytiotrophoblast, and the endothelium of the blood vessels of the primary and secondary villi. 57 In addition, ACE2 and Ang-(1-7) are expressed in the maternal stromal in the invading and intravascular trophoblast and the decidual cells. The similar localization of Ang-(1-7) and ACE2 in the placenta strongly suggests that ACE2 is involved in the processing of Ang-(1-7) in local tissue expression of the peptide.…”

Section: An Additional Perspectivementioning

confidence: 99%

Angiotensin-Converting Enzyme 2 and Angiotensin-(1-7)

2006

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Abstract-This lecture summarizes the chronology and rationale that led to the discovery of angiotensin-(1-7) as a hormone that, in its own right, opposes the vasoconstrictor and proliferative actions of angiotensin II. The work discussed here additionally analyzes the newest findings on angiotensin-converting enzyme 2, the angiotensin-converting enzyme homologue that efficiently hydrolyzes angiotensin II into angiotensin-(1-7). Both components of this system may significantly influence our future perspective of the role of the renin-angiotensin system, not just in terms of its role in the regulation of cardiovascular and renal function but, moreover, as regulators of a vast array of disease processes in which inflammation and immune mechanisms play a role.

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“…During normal pregnancy, bioactive components of the RAS are elevated in the plasma and urine, including Ang-(1-7) (Valdes et al 2001;Merrill et al 2002), and Ang-(1-7) and ACE2 are both expressed in the placenta (Valdes et al 2006). Preeclampsia, a condition that can occur during pregnancy and is characterized by high blood pressure and proteinuria, can be detrimental to both the mother and fetus.…”

Section: Ang-(1-7) and Pregnancymentioning

confidence: 99%

Angiotensin‐(1‐7): Pharmacology and New Perspectives in Cardiovascular Treatments

Trask

Ferrario

2007

Cardiovascular Drug Reviews

101

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Many advances have been made in the cardiovascular field in the last several decades. Among them is the progress completed to date on the heptapeptide member of the reninangiotensin system (RAS), angiotensin-(1-7) [Ang-(1-7)]. The peptide's beneficial actions against pathophysiological processes, such as cardiac arrhythmia, heart failure, hypertension, renal disease, preeclampsia, and even cancer are continuously being uncovered. This review encompasses the pharmacology of Ang-(1-7) and expounds upon the peptide's potential as a therapeutic agent against pathological processes both within and outside the cardiovascular continuum.

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Distribution of Angiotensin-(1-7) and ACE2 in Human Placentas of Normal and Pathological Pregnancies

Cited by 243 publications

References 37 publications

Endothelial Dysfunction

Endothelial Dysfunction

Angiotensin-Converting Enzyme 2 and Angiotensin-(1-7)

Angiotensin‐(1‐7): Pharmacology and New Perspectives in Cardiovascular Treatments

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