Abstract

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.

Methods: The human kidney tissue were collected from patients suffered renal tumor (n: 5) or chronic renal insufficiency (n: 25). The human placental tissues were collected from woman with normal pregnancies (n: 35) and gestational hypertension (n: 21). There is no significant difference in maternal age between normal and gestational hypertension subjects. All the participants received written information, and signed the consent.

Results: Before delivery, the circulating PRL and Ang II concentration in the gestational hypertension is significantly lower than that in normal pregnancy. There is no significant difference between gestational hypertension and normal pregnancy after delivery. In the local RAS, AT1, Ang II and Ang 1-7 levels in gestational hypertension placenta were significantly higher than normal pregnancy. There is no statistical difference of renin, AGT, and ACE, ACE2 between the two subjects.

Conclusion: The change of Ang (1-7) expression in our study is different from the previous studies in preeclampsia. More attention should be put on the balance of Ang II and Ang (1-7).

Keywords: Gestational hypertension; Pregnancy; Renin-angiotensin system; Blood pressure; Vascular endothelial growth factor; cAMP responsive element binding protein

Abbreviations: RAS: Renin-Angiotensin System; AGT: Angiotensinogen; Ang-I: Antiotensin-I; ACE: Angiotensin-Converting Enzyme; Ang II: Angiotensin- II; Ang (1-7): Antiotensin (1-7); CREB: cAMP Responsive Element Binding protein; BP: Blood Pressure; CRI: Chronic Renal Insufficiency; VEGF: Vascular Endothelial Growth Factor; AT1: Angiotensin II receptor type 1; PRL: Renin Activity