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. Copyright 2007 S. Karger AG, Basel.
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 hypertensiverats (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. Copyright 2007 S. Karger AG, Basel.
Authors: Shruti Sharma; Angela Aramburo; Ruslan Rafikov; Xutong Sun; Sanjiv Kumar; Peter E Oishi; Sanjeev A Datar; Gary Raff; Kon Xoinis; Gohkan Kalkan; Sohrab Fratz; Jeffrey R Fineman; Stephen M Black Journal: Pediatr Res Date: 2013-04-29 Impact factor: 3.756
Authors: Maria Giovanna Scioli; Pietro Lo Giudice; Alessandra Bielli; Valeria Tarallo; Alfonso De Rosa; Sandro De Falco; Augusto Orlandi Journal: PLoS One Date: 2015-10-16 Impact factor: 3.240