Effect of L-carnitine and propionyl-L-carnitine on endothelial function of small mesenteric arteries from SHR

  • J Vasc Res. 2007;44(5):354-64. doi: 10.1159/000102303.
Maria Alvarez de Sotomayor  1 ,  Rosario Bueno ,  Concepción Pérez-Guerrero ,  Maria Dolores Herrera
Affiliations
  • 1. Department of Pharmacology, Faculty of Pharmacy, University of Seville, Seville, Spain. [email protected]
PMID: 17483601 DOI: 10.1159/000102303
Abstract

Background: The effect of treatment with either 200 mg x kg(-1) of L-carnitine (LC) or propionyl-L-carnitine (PLC) was studied on endothelial dysfunction of small mesenteric arteries (SMA) from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats.

Methods: Systolic blood pressure (SBP) was measured and endothelial and vascular functions were assessed by the effect of carbachol (CCh) and phenylephrine (Phe). O2- produced by SMA and eNOS expression were evaluated by chemiluminescence and Western blot, respectively.

Results: Although SBP was not affected, endothelial relaxation increased in both LC- and PLC-treated SHR. Nevertheless, the CCh-induced contraction remained sensitive to indomethacin in these rats. On the contrary, NO participation was increased in all the groups except for LC-treated WKY. Furthermore, high concentrations of Phe produced NO-dependent relaxation of SMA from PLC-treated rats. Both compounds decreased basal and NADPH-stimulated O2- in SHR toward values observed in WKY. Only PLC increased eNOS protein expression in SHR. Neither LC nor PLC affected endothelium-derived hyperpolarizing factor-induced relaxation.

Conclusions: LC and its propionate improved endothelial responses of SMA from SHR by decreasing O2- production and thus increasing NO availability. PLC also increased NO synthesis by enhancing eNOS expression.

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