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Overexpression of Angiotensin (1–7) – fusion protein attenuates monocrotaline (MCT) ‐ induced pulmonary hypertension

Pulmonary hypertension is a progressive disease characterized by increased resistance to pulmonary blood flow. Our lab has previously demonstrated that ACE2 overexpression in the lungs of mice attenuated pulmonary pressure in monocrotaline (MCT) model of pulmonary hypertension. We therefore, wanted to investigate the effects of overexpression of Angiotensin (1–7) (Ang (1–7)), a product of ACE2 enzyme, in MCT‐induced rat model of pulmonary hypertension. Lentivirus producing Ang (1–7) ‐ fusion protein was injected into the right ventricle of male SD rats (250–300g). After two weeks of gene transfer, pulmonary hypertension was induced with subcutaneous injection of MCT (45mg/kg). After 4 weeks of MCT administration, rats were instrumented to measure right ventricular systolic pressure (RVSP) followed by heart excision to measure right ventricular hypertrophy. No significant difference in systemic blood pressure (tail cuff) was observed between the different treatment groups (control, 118 ± 6, MCT, 118 ± 3, MCT+Ang (1–7), 123 ± 4). However, MCT administration caused a significant increase in RVSP (MCT, 40 ± 4 mmHg, control 25 ± 2 mmHg, P<0.05) which was attenuated with Ang (1–7) treatment (28 ± 0.2 P<0.05 Vs MCT). MCT administration at the above dose and time period failed to induce right ventricular hypertrophy. We conclude that Ang (1–7) may hold therapeutic potential in the treatment of pulmonary hypertension.