Abstract
The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.7% vessels in 155 tests, as referenced to KCl-induced contractions. In contrast, phenylephrine only produced contractions in 3.0% of 133 tests. In non-placental vessels, phenylephrine induced contractions in 76.0% of 67 tests, whereas angiotensin II failed to produce contractions in 75 tests. Similar results were obtained in animal placental and non-placental vessels. Compared with non-placental vessels, angiotensin II receptors and β -adrenoceptors were significantly increased in placental vessels. Compared to the vessels from normal pregnancy, angiotensin II-induced vasoconstrictions were significantly reduced in preeclamptic placentas, which was associated with a decrease in angiotensin II receptors. In addition, angiotensin II and angiotensin converting enzyme in the maternal-placenta circulation in preeclampsia were increased, whereas angiotensin I and angiotensin1-7 concentrations were unchanged. The study demonstrates a selective effect of angiotensin II in maintaining placental vessel tension, which may play an important role in development of hypertension in preeclampsia.
Highlights
Preeclampsia is an important clinical problem, yet the etiology remains unclear
These results demonstrated that placental vascular responses to Angiotensin II (AII) were significantly more sensitive than those of the non-placental vessels in humans
The present study reveals several important findings: compared to non-placental vessels, vasoconstrictions induced by AII were much stronger than those by catecholamines in both human and animal placental vessels; compared to normal pregnancy (NP), placental vascular responses to AII were decreased in preeclampsia, which was associated with a decrease in AII receptors; AII and Angiotensin converting enzyme (ACE) were significantly increased in the maternal-placental circulation in preeclampsia
Summary
Preeclampsia is an important clinical problem, yet the etiology remains unclear. The placenta plays a critical role in the development of preeclampsia because delivery of the placenta and fetus is the only known efficient approach to resolve hypertension. The regulatory mechanisms of placental vascular dysfunction and their contributions to the development of hypertension in preeclampsia are unclear. Our recent study has demonstrated that placental vascular trees behave very differently from non-placental vessels, with very limited endothelial functions, and dysfunction in vascular smooth muscle cells may play a critical role in development of hypertension www.impactjournals.com/oncotarget in preeclampsia [7]. Placental vascular dysfunction is likely an important cause for impaired placental blood flow in preeclampsia, physiological and pathophysiological activities of placental vessels under normal and preeclamptic conditions remain unclear. We seek to reveal special features of placental vascular regulations and the pathophysiological changes under the preeclamptic condition, and to understand possible contributions of placental vascular dysfunction in the development of hypertension in preeclampsia
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