Effect of estradiol on bradykinin-induced vasoconstriction in ovariectomized rat aorta

[Speaker] Karla S. Dominguez-Romero:1
[Co-author] Ricardo Celedon-Murillo:1, Maria E. Hernandez-Campos:1, Ignacio Valencia-Hernandez:1
1:Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, Instituto Politecnico Nacional, Mexico

Among other changes, menopause is characterized by ovarian hormones deficiency and it can contribute to the development of high blood pressure (HBP), the main cause of morbimortality worldwide. Estrogens can confer cardiovascular protection by reducing the angiotensin-converting enzyme (ACE) activity and the angiotensin II syntesis and preventing the degradation of bradykinin which produces vasodilatation mediated by the activation of B2 receptors and the nitric oxide (NO) sythesis from L-arginine, a reaction catalyzed by the nitric oxide synthase. However, bradykinin under certain conditions produces vasoconstriction, a less studied effect. Therefore, the objective of this work was to study the 17- beta estradiol (E2) effect on bradykinin-induced reactivity changes in aortic rings from ovariectomized rats (OVX). Two groups of Wistar rats were used, sham operated (SHAM) and OVX animals. After 14 days of recovery, E2 (5microg/Kg/day s.c. for 5 days) of corn oil (vehicle) were administred. At the end of the treatment, rats were sacrificed and aortic rings with and whitout endothelium were obtained and in them concentration - response curves to bradykinin, both in the absence or in the presence of L-NAME, were perfomed. The results show that the ovariectomy caused a diestrus phase corroborated using vaginal cytology at the end of the recovery period, which progresses to a estrus phase after E2 treatment. The uterine length was lower in the OVX group than in that from the SHAM group (3.5+-0.26, 5.8+-0.4 for OVX and SHAM groups respectively, P <0.05). The uterine weight did not have significant changes for both groups. Bradykinin induced a concentration-dependent contractile effect that was greater in presence of L-NAME and in the absence of endothelium. Treatment with E2 restores the reactivity to bradykinin. In conclusion, bradykinin produces a vasoconstrictor effect modulated by the endothelium and by NO and treatment with E2 restores the vasoconstrictor response to bradykinin to that obtained in aortic rings from SHAM group.
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