Key result
Mas deletion in pregnant mice produced a preeclampsia-like phenotype with higher diastolic blood pressure at day 19 of pregnancy compared to wild-type mice (90.5 vs 80.3 mmHg, P<0.0001).
Why the study?
Imbalance in the RAS between Ang II/AT1 and Ang-(1-7)/Mas axis is implicated in preeclampsia, but whether reduced Ang-(1-7)/Mas activity directly contributes remained to be determined.
Does G-protein-coupled receptor MAS deletion produce a preeclampsia-like phenotype in pregnant FVB/N mice?
Does G-protein-coupled receptor MAS deletion produce a preeclampsia-like phenotype in pregnant FVB/N mice?
Mas deletion in mice produces a preeclampsia-like state characterized by hypertension, fetal growth restriction, and proteinuria during pregnancy, suggesting a role for the Ang-(1-7)/Mas axis in preeclampsia.
Mas receptor deletion induces preeclampsia-like features in mice; hypothesis-generating for Ang-(1-7)/Mas pathway in human gestational hypertension.
BACKGROUND: An unbalance in the renin-angiotensin (Ang) system (RAS) between the Ang II/AT1 and Ang-(1-7)/Mas axis appears to be involved in preeclampsia (PE), in which a reduction in Ang-(1-7) was observed. Here, we tested whether the reduction in the activity of the Ang-(1-7)/Mas axis could be a contributing factor for the development of PE, using Mas-deficient (Mas-/-) mice. METHODS AND RESULTS: Cardiovascular parameters were evaluated by telemetry before, during pregnancy and 4 days postpartum in 20-week-old Mas-/- and wild-type (WT) female mice. Mas-/- mice presented reduced arterial blood pressure (BP) at baseline (91.3 ± 0.8 in Mas-/- vs. 94.0 ± 0.9 mmHg in WT, Diastolic, P<0.05). However, after the 13th day of gestation, BP in Mas-/- mice started to increase, time-dependently, and at day 19 of pregnancy, these animals presented a higher BP in comparison with WT group (90.5 ± 0.7 in Mas-/- vs. 80.3 ± 3.5 mmHg in WT, Diastolic D19, P<0.0001). Moreover, pregnant Mas-/- mice presented fetal growth restriction, increase in urinary protein excretion as compared with nonpregnant Mas-/-, oliguria, increase in cytokines, endothelial dysfunction and reduced ACE, AT1R, ACE2, ET-1A, and eNOS placental mRNA, similar to some of the clinical manifestations found in the development of PE. CONCLUSIONS: These results show that Mas-deletion produces a PE-like state in FVB/N mice.
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Pimentel et al. (2023) studied Preeclampsia. Mas deletion (Mas-/-) vs. Wild-type (WT) mice was evaluated on Diastolic blood pressure at day 19 of pregnancy (mmHg) (p=<0.0001). Mas deletion in pregnant mice produced a preeclampsia-like phenotype with higher diastolic blood pressure at day 19 of pregnancy compared to wild-type mice (90.5 vs 80.3 mmHg, P<0.0001).
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