Ang-(1-7) might prevent the development of monocrotaline induced pulmonary arterial hypertension in rats

L. Chen#, J. Xiao#, Y. Li*, H. Ma*

# Division of Cardiology, First Affilliated Hospital Of Kunming Medical College, Cardiovascular Research Institute, Xichang Road 295, Kunming (China) *Division of Cardiology, First Affiliated Hospital, Cardiovascular Research Institute, Sun Yat-sen University, 58 Zhongshan Rd II, Guangzhou (China)

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• Cardiology

Objectives: To investigate whether Angiotensin-(1-7) [Ang-(1-7)] could prevent the development of monocrotaline (MCT) induced pulmonary arterial hypertension and vascular remodeling.

Masterial and Methods: 30 Sprgue-Dawely rats were randomly assigned into three groups: control group,pulmonary arterial hypertension (PAH) group and PAH +Ang-(1-7) group. Rats in PAH group and PAH +Ang-(1-7) group received 60 mg/kg monocrotaline (MCT) injection subcutaneously and after 24 hours received either saline or 24 µg/kg/h of Ang-(1-7) injection via osmotic minipumps for 4 weeks. Those rats in control group were firstly injected saline subcutaneously and then received saline injection via osmotic minipumps.

Results: After four weeks, in PAH group, right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), percentage of wall thickness (WT%) and percentage of wall area (WA%) were significantly increased, and the level of endothelial nitric oxide synthase (eNOS) protein, eNOS ser 1177-phosphorylati, Akt-phosphorylation were significantly decreased compared with control group. However, RVSP, RVHI, WT%, WA% were dramatically decreased in PAH+Ang-(1-7) group and the level of eNOS protein, eNOS ser 1177-phosphorylation, Akt-phosphorylation were significantly increased compared with PAH group.

Conclusion: Those results suggest that Ang-(1-7) could prevent the development of monocrotaline induced pulmonary arterial hypertension and vascular remodeling, which appears to be associated with up-regulation of eNOS activation via Akt pathway.

Corresponding Author: Hong Ma, MD; e-mail: cheng_l_x@sina.com

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