Vasoconstrictively Acting AT1R A1166C and NOS3 4/5 Polymorphisms in Recurrent Spontaneous Abortions (RSA)*

Authors


  • *

    Respectfully dedicated to our chairman, Prof. Dr med Herrmann Hepp, for his 70th birthday.

Address reprint requests to Christian J. Thaler, Department of Obstetrics and Gynecology – Großhadern, Klinikum der Universität München, D-81377 München, Germany.
E-mail: thaler@med.uni-muenchen.de

Abstract

Problem:  Inadequate uteroplacental perfusion is one of the main reasons for recurrent spontaneous abortions (RSA). Coagulation, fibrinolysis, and vasoconstriction affect tissue perfusion. These systems are regulated by different gene products. Polymorphisms can modulate the expression levels of the respective genes and can thereby affect perfusion. Vasoconstriction is influenced by the expression of endothelial nitric oxide synthase (eNOS) and of the angiotensinogen II type 1 receptor (AT1R).

Method:  The aim of our study was to investigate, whether two polymorphisms in the AT1R and NOS3 genes shown to result in maternal vasoconstriction are associated with an increased risk for RSA.

Results:  Our data indicate that the vasoconstrictively acting genotypes AT1R C/C and NOS3 4/4 are of similar prevalence in RSA patients and in controls.

Conclusion:  Results do not show any influence of the polymorphisms studied on early pregnancy development. This is in concordance with the concept of an independent regulation of placental perfusion.

Ancillary