Augmented endothelial l-arginine transport ameliorates pressure-overload-induced cardiac hypertrophy

Niwanthi W Rajapakse, Tamara Johnston, Helen Kiriazis, Jaye P F Chin-Dusting, Xiao-Jun Du, David M Kaye

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)


NEW FINDINGS: What is the central question of this study? What is the potential role of endothelial NO production via overexpression of the l-arginine transporter, CAT1, as a mitigator of cardiac hypertrophy? What is the main finding and its importance? Augmentation of endothelium-specific l-arginine transport via CAT1 can attenuate pressure-overload-dependent cardiac hypertrophy and fibrosis. Our findings support the conclusion that interventions that improve endothelial l-arginine transport may provide therapeutic utility in the setting of myocardial hypertrophy. Such modifications may be introduced by exercise training or locally delivered gene therapy, but further experimental and clinical studies are required. Endothelial dysfunction has been postulated to play a central role in the development of cardiac hypertrophy, probably as a result of reduced NO bioavailability. We tested the hypothesis that increased endothelial NO production, mediated by increased l-arginine transport, could attenuate pressure-overload-induced cardiac hypertrophy. Echocardiography and blood pressure measurements were performed 15 weeks after transverse aortic constriction (TAC) in wild-type (WT) mice (n = 12) and in mice with endothelium-specific overexpression of the l-arginine transporter, CAT1 (CAT+; n = 12). Transverse aortic constriction induced greater increases in heart weight to body weight ratio in WT (by 47 ) than CAT+ mice (by 25 ) compared with the respective controls (P
Original languageEnglish
Pages (from-to)796 - 804
Number of pages9
JournalExperimental Physiology
Issue number7
Publication statusPublished - 2015

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