l-carnitine and its propionate: Improvement of endothelial function in SHR through superoxide dismutase-dependent mechanisms

• Published in: Free radical research 2007-01, Vol.41 (8), p.884-891
• Main Authors: Alvarez de Sotomayor, Maria, Mingorance, Carmen, Rodriguez-Rodriguez, Rosalía, Marhuenda, Elisa, Herrera, Maria Dolores
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants - pharmacology; Blood Pressure; Carnitine - analogs & derivatives; Carnitine - pharmacology; Cu/Zn-SOD; Endothelium, Vascular - drug effects; Endothelium, Vascular - enzymology; eNOS; Hypertension - metabolism; l-carnitine; Male; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - metabolism; Nitric Oxide Synthase Type III - antagonists & inhibitors; Nitric Oxide Synthase Type III - metabolism; propionyl-l-carnitine; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Reactive Oxygen Species - metabolism; superoxide; Superoxide Dismutase - metabolism; Superoxides - metabolism
• ISSN: 1071-5762; 1029-2470
• DOI: 10.1080/10715760701416467

To clarify the mechanism underlying the antioxidant properties of l-carnitine (LC) and propionyl-l-carnitine (PLC) on spontaneously hypertensive (SHR) and normotensive WKY, animals were treated with either PLC or LC (200 mg kg− 1). Aorta was dissected and contraction to (R)-( − )-phenylephrine (Phe) and relaxation to carbachol (CCh) were assessed in the presence or not of the NO synthase (NOS) inhibitor, l-NAME. O _{2}^{\z.rad - } production was evaluated by lucigenin-enhanced chemiluminescence and its participation on relaxation was observed after incubation with superoxide dismutase (SOD) plus catalase. Protein expressions of eNOS, Cu/Zn-SOD and Mn-SOD were studied by western blot. Both LC and PLC treatments improved endothelial function of SHR through increasing NO participation and decreasing O _{2}^{\z.rad - } probably involving higher Cu/Zn-SOD expression. PLC treatment augmented eNOS expression in SHR. Surprisingly, LC increased O _{2}^{\z.rad - } produced by aorta from WKY and thus diminished NO and damaged endothelial function. Conversely, PLC did not affect CCh-induced relaxation in WKY. These results demonstrate that LC and PLC prevent endothelial dysfunction in SHR through an antioxidant effect.