The upregulation of angiotensin II receptor AT1 in human preeclamptic placenta

Po Sing Leung, Shaw Jenq Tsai, Gerd Wallukat, Tse Ngong Leung, Tze Kin Lau

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The human placenta has been considered to possess a locally generated renin-angiotensin system (RAS), which may play a physiological role in the regulation of uteroplacental blood circulation. The changes in the expression of such a placental RAS during pregnancy could be important for the physiological and pathophysiological aspects of some clinical disorders, such as pregnancy-induced hypertension, preeclampsia. In the present study, the alterations of expression and localization of placental angiotensin II receptor subtypes, namely AT1 in patients with preeclampsia (elective caesarean delivery) were investigated and compared with controls (vaginal delivery and elective caesarian delivery) using semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR), Western blot and immunohistochemistry respectively. Results from RT-PCR analysis revealed an upregulated expression of placental mRNA for AT1 receptor subtype in patients with preeclampsia when compared with those in controls. In addition, there was also a significant activation of placental expression of angiotensinogen mRNA in patients with preeclampsia. Results from Western blot showed that the expression of AT1 receptor was also upregulated. Immunohistochemical results further demonstrated that increased immunoreactivity for placental AT1 receptor was predominantly localized to the thin layers of syncytiotrophoblasts and, to a less extent, the capillaries of the term placental villi. These data indicate that upregulation of placental RAS components, notably AT1 receptor in the syncytiotrophoblasts, could play a pathophysiological role in patients with preeclampsia.

Original languageEnglish
Pages (from-to)95-102
Number of pages8
JournalMolecular and Cellular Endocrinology
Issue number1-2
Publication statusPublished - 2001 Nov 26

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Endocrinology


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