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Cardiovascular Research 1998 37(3):756-764; doi:10.1016/S0008-6363(97)00295-2
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Chronic dietary supplementation with L-arginine inhibits platelet aggregation and thromboxane A2 synthesis in hypercholesterolaemic rabbits in vivo

Stefanie M Bode-Böger*, Rainer H Böger, Sven Kienke, Michael Böhme, Laddaval Phivthong-ngam, Dimitrios Tsikas and Jürgen C Frölich

Institute of Clinical Pharmacology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany

* Corresponding author. Tel.: +49 (511) 5324631; fax: +49 (511) 5325199.

Objectives: L-arginine exerts anti-atherosclerotic effects in hypercholesterolaemic rabbits via modulating endogenous NO production. We investigated whether L-arginine inhibits thromboxane formation in vivo and platelet aggregation ex vivo in this animal model. Methods: The urinary excretion rates of 2,3-dinor-6-keto-PGF1{alpha} (major urinary metabolite of PGI2) and 2,3-dinor-TXB2 (major urinary metabolite of thromboxane A2) were used as indicators of platelet–endothelial cell interactions in vivo. Rabbits were fed 1% cholesterol (Cholesterol group, N=8), 1% cholesterol plus 2,25% L-arginine (Cholesterol+L-arginine, N=8), or normal rabbit chow (Control, N=4) for 12 weeks. Urine samples were collected in weekly intervals. At the end of the study period platelet aggregation ex vivo and endothelium-dependent and -independent vascular function of isolated aortic rings in vitro was assessed. Results: Urinary 2,3-dinor-TXB2 excretion significantly increased in the cholesterol group (p<0.05), and endogenous NO formation (measured as urinary nitrate excretion) decreased (p<0.05). Both parameters were significantly correlated with each other (R=0.48, p<0.01). L-arginine partly restored urinary nitrate excretion and significantly reduced TXA2 production to values even below those in the control group (p<0.001). Urinary 2,3-dinor-6-keto-PGF1{alpha} excretion increased in early hypercholesterolaemia and returned to control values in the second half of the study period. The early increase in urinary 2,3-dinor-6-keto-PGF1{alpha} excretion was attenuated by L-arginine. Platelet aggregation was significantly enhanced in cholesterol-fed rabbits and attenuated by dietary L-arginine. L-arginine also improved the impaired endothelium-dependent relaxations to ADP, and normalized the vasoconstrictor effects of 5-HT in isolated aortic rings. Conclusions: Cholesterol-feeding enhances platelet aggregation and TXA2 formation, and stimulates platelet–endothelial cell interaction in rabbits. These effects are probably due to impaired NO elaboration, as indicated by decreased urinary nitrate excretion. Chronic dietary supplementation with L-arginine elevates systemic NO elaboration and significantly increases the PGI2/TXA2 ratio. It thus beneficially influences the homeostasis between vasodilator and vasoconstrictor prostanoids in vivo.

KEYWORDS Nitric oxide; Prostacyclin; Endothelium; Platelet aggregation; Gas chromatography–mass spectrometry


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