Abstract Title:

L-arginine restores endothelial nitric oxide synthase-coupled activity and attenuates monocrotaline-induced pulmonary artery hypertension in rats.

Abstract Source:

Am J Physiol Endocrinol Metab. 2010 Mar 9. Epub 2010 Mar 9. PMID: 20215577

Abstract Author(s):

Zhi-Jun Ou, Wei Wei, Da-De Huang, Wei Luo, Dan Luo, Zhi-Ping Wang, Xi Zhang, Jing-Song Ou

Article Affiliation:

1The First Affiliated Hospital, Sun Yat-sen University.


L-arginine can attenuate pulmonary hypertension (PH) by a mechanism that are not fully understood. This study investigated the molecule mechanism of L-arginine attenuating PH.Sprague Dawley rats were treated with monocrotaline (MCT) +/- L-arginine for 3 or 5 weeks. Right ventricular systolic pressure (RVSP), right heart hypertrophy, survival rate, pulmonary artery wall thickness, nitric oxide (NO) concentration and superoxide anion (O2(*-)) generation in the lung were measured. Expressions of endothelial nitric oxide synthase (eNOS) and heat shock protein 90 (HSP90), phosphorylation of eNOS at S1177, and the association of eNOS and HSP90 in the lung were determined by western blot and immunoprecipitation experiments. MCT increased RVSP, right heart hypertrophy, mortality, pulmonary artery wall thickness, and O2(*-) generation and decreased eNOS and HSP90 expression and association, phosphorylation of eNOS at S1177, and NO production. L-arginine decreased RVSP, right heart hypertrophy, mortality, O2(*-) generation, and pulmonary artery wall thickness and increased NO production. L-arginine increased eNOS expression, phosphorylation of eNOS at S1177, and association of eNOS and HSP90 without significantly altering HSP90 expression. L-arginine may act through three pathways, providing a substrate for NO generation, preserving eNOS expression/phosphorylation and maintaining the association of eNOS and HSP90, which allows restoration of eNOS activity and coupling activity, to maintain the balance between NO and O2(*-) and delay the development of PH.

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