Previous studies have demonstrated a protective effect of the Ang-(1-7)/Mas receptor axis on pathological cardiac hypertrophy. Also, the involvement of Mas receptor in the exercise-induced cardiac hypertrophy has been suggested. However, the role of the Ang-(1-7)/Mas receptor on pregnancy-induced cardiac remodeling remains unknown. The objective of this study was to evaluate the participation of the Mas receptor in the development of the cardiac hypertrophy and fibrosis induced by gestation. Female Wistar rats were shared in 3 groups: control , pregnant , and pregnant treated with Mas receptor antagonist A-779 . Wild type (WT) and Mas-knockout mice (KO) were distributed in non-pregnant and pregnant groups. Systolic blood pressure (SBP) was measured by tail-cuff plethysmography. The medial part of the left ventricle (LV) was collected for histological analysis. Echocardiographic analysis was used to evaluate the cardiac function. SBP was not changed by pregnancy or A-779 treatment in the Wistar rats. Pharmacological blockade or genetic deletion of Mas receptor attenuates the pregnancy-induced myocyte hypertrophy. The treatment with A-779 or genetic deletion of the Mas receptor increased the collagen III deposition in LV from pregnant animals without changing the fibroblast proliferation. KO mice presented a lower ejection fraction, fraction shortening, stroke volume and higher end systolic volume compared to WT. Interestingly, the pregnancy restored these parameters. In conclusion, these data show that while Mas receptor blockade or deletion decreases physiological hypertrophy of pregnancy, it is associated with more extracellular matrix deposition. These alterations are associated with improvement of the cardiac function through Mas-independent mechanism.
- Cardiac hypertrophy
- Heart function
- Mas Receptor
- ©2016 The Author(s)
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