Alterations in the 'local umbilical cord blood renin-angiotensin system' during pre-eclampsia

Abstract

Background: Local autocrine-paracrine renin-angiotensin system (RAS), independently functioning from the circulating RAS, is present in major organs of the female reproductive tract. We have previously demonstrated 'a local RAS in human umbilical cord' via verifying the corresponding ACE, renin, and angiotensinogen mRNAs. The aim of this study is to search alterations of the local umbilical cord RAS during pre-eclampsia.

Methods: Cord blood samples were obtained from 19 patients with pre-eclampsia (aged mean 26.6 ± 5.83 (range 18-42) years) and 20 women with normal pregnancy (aged mean 28.26 ± 7.30 (range 19-37) years). Women with uncomplicated pregnancy formed the control group. Real time quantitative PCR analysis for ACE, renin and angiotensinogen gene expressions were carried out using a LightCycler™ instrument.

Results: The mean expression ratios were 0.0029 ± 0.0015 for renin, 0.153 ± 0.166 for angiotensinogen, and 0.220 ± 0.294 for ACE, in control samples. The mean expression ratios of pre-eclamptic patients were 0.0061 ± 0.00068, 0.035 ± 0.008, and 0.030 ± 0.006 for renin, angiotensinogen and ACE genes, respectively. While renin expressions increased in the local cord blood of pre-eclampsia in comparison to the normal cord blood, unpredictable decrements in the angiotensinogen and ACE expressions were observed within the same pre-eclamptic samples. There were no statistically significant differences between intrauterine growth restriction (IUGR) and appropriate for gestational age (AGA) newborns in respect to renin, angiotensinogen and ACE gene expressions.

Conclusions: These findings indicate that the gene expression in the major components of the local RAS does not represent a constant mathematical model, but is affected from the ongoing pathobiological events associated with the disease course. Local umbilical cord blood RAS alterations at the basis of genetic expression are evident in pre-eclampsia.