Title:The Functional Role of the Renin-Angiotensin System in Preeclampsia
Volume: 19
Issue: 3
Author(s): Leta Melaku*
Affiliation:
- Department of Biomedical Sciences, College of Health Sciences, Arsi University, Asella, Oromia, Ethiopia
Keywords:
RAS, ACE, ACE 2, angiotensin II, angiotensin 1-7, prorenin, renin, AT1 receptor autoantibodies, aldosterone, preeclampsia.
Abstract: The renin-angiotensin system (RAS) is a signaling pathway that acts as a major regulator
in human physiology. To sidestep the major intimidations of low blood volume and low blood pressure,
the diverse actions of Ang II/ACE/AT1R can be viewed as a useful response in maintaining
homeostasis. The deleterious action of the Ang II/ACE/AT1R axis is endogenously counterbalanced
by ACE 2/Ang 1-7/MasR. Yet, over activation of the Ang II/ACE/AT1R axis may lead to hypertension.
Preeclampsia is characterized by hypertension with proteinuria or end-organ dysfunction after
20 weeks of gestation. The early-onset sort is more genuine and capable of high maternal and fetal
dismalness and mortality rates than the late-onset sort of preeclampsia. Various theories for the
pathogenesis of preeclampsia are, the exact underlying molecular mechanisms remain unclear but
are likely to be multifactorial. Later studies of RAS in preeclampsia have highlighted the need for
thorough research on this topic. There is an increase in the levels of circulating angiotensinogen during
the first 20 weeks of gestation. At the beginning of the pregnancy, there is an increment of prorenin
by 4 - 5 times. Renin synthesis in preeclampsia is suppressed. PE pregnant women have higher
levels of prorenin receptor expression in their placental tissue than normal pregnant women. AT1
receptor autoantibodies are also observed. Ang II is raised in normal pregnancies as a result of higher
levels of angiotensinogen and renin. Preeclampsia causes a decrease in angiotensin-(1-7) levels.
Aldosterone is also relatively low in pregnancies complicated by preeclampsia.
